InR and Pi3K maintain intestinal homeostasis through STAT/EGFR and Notch signaling in enteroblasts.

To maintain the integrity of the adult gut, the proliferation and differentiation of stem cells must be strictly controlled. Several signaling pathways control the proliferation and differentiation of Drosophila intestinal epithelial cells. Although the modulatory effects of insulin pathway components on cell proliferation have been characterized, their specific role in which cell type and how these components interact with other regulatory signaling pathways remain largely unclear. In this study, we found that InR/Pi3K has major functions in enteroblasts (EBs) that were not previously described. The absence of InR/Pi3K in progenitors leads to a decrease in the number of EBs, while it has no significant effect on intestinal stem cells (ISCs). In addition, we found that InR/Pi3K regulates Notch activity in ISCs and EBs in an opposite way. This is also the reason for the decrease in EB. On the one hand, aberrantly low levels of Notch signaling in ISCs inhibit their proper differentiation into EBs; on the other hand, the higher Notch levels in EBs promote their excessive differentiation into enterocytes (ECs), leading to marked increases in abnormal ECs and decreased proliferation. Moreover, we found that Upd/JAK/STAT signaling acts as an effector or modifier of InR/Pi3K function in the midgut and cooperates with EGFR signaling to regulate cell proliferation. Altogether, our results demonstrate that InR and Pi3K are essential for coordinating stem cell differentiation and proliferation to maintain intestinal homeostasis.

Training intensity of robot-assisted gait training in children with cerebral palsy.

AIM: We compared three different intensities of robot-assisted gait training (RAGT) for achieving favourable outcomes in children with cerebral palsy (CP). METHOD: This study was conducted using a randomized controlled, single-blind design. Thirty children (19 males and 11 females; mean age 6 years 1 month, SD 2 years) with CP classified in Gross Motor Function Classification System levels II and III were assigned to three different RAGT intensity groups: high-intensity (fastest walking speed and lowest body weight support [BWS]), low-intensity (slowest speed and highest BWS), and comfortable intensity (intermediate speed and intermediate BWS). The RAGT intervention was performed three times a week for 6 weeks. Outcome measures included the 88-item Gross Motor Function Measure, stability index, spatiotemporal parameters of gait analysis, paediatric functional independence measure, and the Canadian Occupational Performance Measure. RESULTS: The 88-item Gross Motor Function Measure was significantly improved after training in the high-intensity (D Δ8.3 ± 15.6; E Δ3.8 ± 4.1) and comfortable intensity (D Δ2.9 ± 3.1; E Δ1.2 ± 2.0) groups, whereas gait speed was improved in the comfortable intensity group, without statistically significant group differences. Only the low-intensity group showed improvement on the stability index (Δ -0.6 ± 0.9, p = 0.05). Everyday functional performance significantly improved in all three groups, with the comfortable intensity group showing the greatest improvement. INTERPRETATION: Different training intensities produced improvement in different areas; individualized RAGT intensity adjustment is therefore needed based on the rehabilitation goal.

Inonotus obliquus aqueous extract inhibits intestinal inflammation and insulin metabolism defects in Drosophila.

In biomedical research, the fruit fly (Drosophila melanogaster) is among the most effective and flexible model organisms. Through the use of the Drosophila model, molecular mechanisms of human diseases can be investigated and candidate pharmaceuticals can be screened. White rot fungus Inonotus obliquus is a member of the family Hymenochaetaceae. Due to its multifaceted pharmacological effects, this fungus has been the subject of scientific investigation. Nevertheless, the precise mechanisms by which Inonotus obliquus treats diseases remain unclear. In this study, we prepared an aqueous extract derived from Inonotus obliquus and demonstrated that it effectively prevented the negative impacts of inflammatory agents on flies, including overproliferation and overdifferentiation of intestinal progenitor cells and decreased survival rate. Furthermore, elevated reactive oxygen species levels and cell death were alleviated by Inonotus obliquus aqueous extract, suggesting that this extract inhibited intestinal inflammation. Additionally, Inonotus obliquus aqueous extract had an impact on the insulin pathway, as it alleviated growth defects in flies that were fed a high-sugar diet and in chico mutants. In addition, we determined the composition of Inonotus obliquus aqueous extract and conducted a network pharmacology analysis in order to identify prospective key compounds and targets. In brief, Inonotus obliquus aqueous extract exhibited considerable potential as a therapeutic intervention for human diseases. Our research has established a foundational framework that supports the potential clinical implementation of Inonotus obliquus.

The protective effect of safranal against intestinal tissue damage in Drosophila.

Drosophila is often exposed to harmful environments, and the intestinal epithelium is the first line of defense against external infection. Intestinal stem cells (ISCs) in the Drosophila midgut play a crucial role in maintaining tissue homeostasis and compensating for cell loss caused by tissue damage. Crocus sativus L. (saffron) can protect against intestinal injury in response to inflammation; however, the specific protective components of saffron and the related mechanisms remain unclear. Safranal is one of the main components of saffron. Here, we used dextran sodium sulfate (DSS) or Erwinia carotovora carotovora 15 (Ecc15) to create an intestinal injury model and explored the protective effect of safranal against tissue damage. Excessive proliferation and differentiation of ISCs in the Drosophila midgut were observed after DSS or Ecc15 feeding; however, these phenotypes were rescued after safranal feeding. In addition, we found that this process occurred through inhibition of the c-Jun N-terminal kinase (JNK), epidermal growth factor receptor (EGFR) and Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways. Furthermore, safranal inhibited the Ecc15- and DSS-induced increases in antimicrobial peptide (AMP) and reactive oxygen species (ROS) levels and intestinal epithelial cell death, thereby protecting gut integrity. In summary, safranal was found to have a significant protective effect and maintain intestinal homeostasis in Drosophila; these findings provide a foundation for the application of safranal in clinical research and the treatment of intestinal injury.

Acanthopanax senticosus polysaccharide regulates the intestinal homeostasis disruption induced by toxic chemicals in Drosophila.

The intestinal epithelium provides the first line of defense against pathogens and toxic compounds. The ingestion of toxic compounds causes an enhanced epithelial cell death and an excessive proliferation of intestinal stem cells, eventually resulting in the disruption of gut homeostasis. In this study, Drosophila gut inflammation model induced by toxic compounds was exploited to analyze the ameliorative effect of Acanthopanax senticosus polysaccharide on the disruption of gut homeostasis. As a result, it was found that A. senticosus polysaccharide can significantly increase the survival rate of Drosophila adults as well as reduce the excessive proliferation and differentiation of intestinal stem cells through epidermal growth factor receptor, jun-N-terminal kinase, and Notch signaling pathways under the exposure to toxic compounds dextran sodium sulfate. Moreover, the polysaccharide effectively decreased the epithelial cell death and the accumulation of reactive oxygen species and antimicrobial peptides induced by sodium dodecyl sulfate. In addition, it was found that A. senticosus polysaccharide can extend the lifespan of only female flies but not male flies. In conclusion, A. senticosus polysaccharide has an obvious protective effect on the gut homeostasis of Drosophila melanogaster.

Drosophila jumu modulates apoptosis via a JNK-dependent pathway and is required for other processes in wing development.

Previous studies in several model organisms have revealed that members of the Forkhead (Fkh) transcription factor family have multiple functions. Drosophila Jumeau (Jumu), a member of this family, participates in cardiogenesis, hematopoiesis and immune system homeostasis. Here, we show that loss of jumu function positively regulates or triggers apoptosis via a JNK-dependent pathway in wing development. jumu mutants showed reduced wing size and increased apoptosis. Moreover, we observed a loss of the anterior cross vein (ACV) phenotype that was similar to that observed in wings in which JNK signaling has been ectopically activated. The JNK signaling markers puckered (puc) and p-JNK were also significantly increased in the wing discs of jumu mutants. In addition, apoptosis induced by the loss of jumu was rescued by knocking down JNK, indicating a role for JNK in reducing jumu-induced apoptosis. Jumu could also control wing margin development via the positive regulation of cut expression, and the observed wing margin defect did not result from a loss of jumu-induced apoptosis. Further, jumu deficiency in the pupal wing could induce multiple wing hairs via a Rho1-mediated planar cell polarity pathway, but abnormal Rho1 expression was not why jumu loss induced apoptosis via a JNK-dependent pathway in wing discs.

A high-sugar diet affects cellular and humoral immune responses in Drosophila.

A high-sugar diet (HSD) induces Type 2 diabetes (T2D) and obesity, which severely threaten human health. The Drosophila T2D model has been constructed to study the mechanisms of insulin resistance, diet-induced cardiovascular diseases and other conditions. Innate immunity is the first line of defense against invading pathogens and parasites. However, few studies have focused on the relationship between a HSD and the innate immune response in Drosophila. In this study, we fed flies a high-sucrose diet and observed defects in the phagocytosis of latex beads and B. bassiana spores. The actin cytoskeleton was also disrupted in hemocytes from HSD-fed larvae. Furthermore, HSD induced the differentiation of lamellocytes in the lymph gland and circulating hemolymph, which rarely occurs in healthy bodies, via JNK signaling. In addition, the Toll and JNK pathways were excessively activated in the fat bodies of HSD-fed larvae, and a large number of dead cells were observed. Finally, HSD induced the aberrant activation of the innate immune system, including inflammation. Our results have established a connection between T2D and the innate immune response.

Jumu is required for circulating hemocyte differentiation and phagocytosis in Drosophila.

BACKGROUND: The regulatory mechanisms of hematopoiesis and cellular immunity show a high degree of similarity between insects and mammals, and Drosophila has become a good model for investigating cellular immune responses. Jumeau (Jumu) is a member of the winged-helix/forkhead (FKH) transcription factor family and is required for Drosophila development. Adult jumu mutant flies show defective hemocyte phagocytosis and a weaker defense capability against pathogen infection. Here, we further investigated the role of jumu in the regulation of larval hemocyte development and phagocytosis. METHODS: In vivo phagocytosis assays, immunohistochemistry, Real-time quantitative PCR and immunoblotting were performed to investigate the effect of Jumu on hemocyte phagocytosis. 5-Bromo-2-deoxyUridine (BrdU) labeling, phospho-histone H3 (PH3) and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining were performed to analyze the proliferation and apoptosis of hemocyte; immunohistochemistry and Mosaic analysis with a repressible cell marker (MARCM) clone analysis were performed to investigate the role of Jumu in the activation of Toll pathway. RESULTS: Jumu indirectly controls hemocyte phagocytosis by regulating the expression of NimC1 and cytoskeleton reorganization. The loss of jumu also causes abnormal proliferation and differentiation in circulating hemocytes. Our results suggest that a severe deficiency of jumu leads to the generation of enlarged multinucleate hemocytes by affecting the normal cell mitosis process and induces numerous lamellocytes by activating the Toll pathway. CONCLUSIONS: Jumu regulates circulating hemocyte differentiation and phagocytosis in Drosophila. Our findings provide new insight into the mechanistic roles of cytoskeleton regulatory proteins in phagocytosis and establish a basis for further analyses of the regulatory mechanism of the mammalian ortholog of Jumu in mammalian innate immunity.

The zinc finger protein CG12744 is essential for differentiation and regeneration after infection in the adult Drosophila midgut.

Pluripotent stem cell activity is essential to maintain regeneration and homeostasis in the Drosophila midgut following environmental challenges. Although multiple pathways have been implicated in epithelial renewal, the underlying regulatory mechanisms and correlations between relevant genes and pathways remain elusive. In this study, we show that the zinc finger protein CG12744 plays an important role in the differentiation and regeneration of epithelial cells in response to oral infection with Erwinia carotovora carotovora 15. Knocking down CG12744 in enteroblasts decreased the post-infection proportion of enteroblasts and enterocytes and increased the post-infection number of enteroendocrine cells. In addition, in precursors, CG12744 affected the Osa, jun-N-terminal kinase and bone morphogenetic protein signaling pathways to control enterocyte differentiation. Finally, CG12744 maintained epithelial architecture and cell fate in enterocytes following an acute infectious challenge.

High sugar diet disrupts gut homeostasis though JNK and STAT pathways in Drosophila.

The incidence of diseases associated with a high sugar diet has increased in the past years, and numerous studies have focused on the effect of high sugar intake on obesity and metabolic syndrome. However, how a high sugar diet influences gut homeostasis is still poorly understood. In this study, we used Drosophila melanogaster as a model organism and supplemented a culture medium with 1 M sucrose to create a high sugar condition. Our results indicate that a high sugar diet promoted differentiation of intestinal stem cells through upregulation of the JNK pathway and downregulation of the JAK/STAT pathway. Moreover, the number of commensal bacteria decreased in the high sugar group. Our data suggests that the high caloric diet disrupts gut homeostasis and highlights Drosophila as an ideal model system to explore gastrointestinal disease.

Tissue-resident stem cell activity: a view from the adult Drosophila gastrointestinal tract.

The gastrointestinal tract serves as a fast-renewing model for unraveling the multifaceted molecular mechanisms underlying remarkably rapid cell renewal, which is exclusively fueled by a small number of long-lived stem cells and their progeny. Stem cell activity is the best-characterized aspect of mucosal homeostasis in mitotically active tissues, and the dysregulation of regenerative capacity is a hallmark of epithelial immune defects. This dysregulation is frequently associated with pathologies ranging from chronic enteritis to malignancies in humans. Application of the adult Drosophila gastrointestinal tract model in current and future studies to analyze the immuno-physiological aspects of epithelial defense strategies, including stem cell behavior and re-epithelialization, will be necessary to improve our general understanding of stem cell participation in epithelial turnover. In this review, which describes exciting observations obtained from the adult Drosophila gastrointestinal tract, we summarize a remarkable series of recent findings in the literature to decipher the molecular mechanisms through which stem cells respond to nonsterile environments.

Ultrasensitive and selective fluorimetric detection of copper ions using thiosulfate-involved quantum dots.

A simple and effective quantum dots (QDs)-based sensing method for copper ion (Cu(2+)) in water is developed with improved selectivity and ultrahigh sensitivity in the presence of thiosulfate. For this, hexadecyl trimethylammonium bromide (CTAB) modified CdSe/ZnS QDs is used as a fluorescent probe. In the absence of thiosulfate, mercury and silver ions show strong interference with Cu(2+) ions even though the sensitivity can be obtained within a few nanomolar. By using our method, the lowest detected concentration for Cu(2+) is 0.15 nM in the presence of thiosulfate in DI water. Also, it is successfully demonstrated for Cu(2+) ion detection in practical application (tap water) down to lowest detection limit, 0.14 nM. This method provides a good potential for copper ions detection with simplicity, rapidity, ultrahigh sensitivity, and excellent selectivity.

Effect of uracil addition on proteomic profiles and 1,3-ß-glucan production in Agrobacterium sp.

Uridine diphosphate (UDP)-glucose is a precursor of 1,3-ß-glucan and is synthesized from glucose-1-phosphate and uridine triphosphate (UTP). Uracil was used as a precursor for UTP, which resulted in an increase in both the UDP-glucose level and the rate of 1,3-ß-glucan synthesis. 1,3-ß-Glucan production metabolism was reactivated after uracil addition during fermentation. 2D-PAGE was used to examine the changes in the expression level of the key metabolic enzymes in the production of 1,3-ß-glucan after uracil addition. The results showed that the expression levels of UTP-glucose-1-phosphate uridylytransferase, phosphoglucomutase, and 1,3-ß-glucan synthase catalytic subunit, key metabolic enzymes in the curdlan biosynthesis pathway, were increased after uracil addition by 3.5%, 30%, and 35%, respectively. Uracil phosphoribosyltransferase, which converts uracil to uridine monophosphate (UMP), was also upregulated 79% more than that without uracil addition. However, the expression levels of orotidine 5-phosphate decarboxylase, glucose-1-phosphate adenylyltransferase, and glucose-6-phosphate isomerase were decreased after uracil addition. This proteomic information is useful for predicting changes in the pathway of uracil utilization. This work provides proteomic information for the integrative analysis of bioinformatic databases, which can be used to predict and understand the metabolism of glucan synthesis at the cellular level.

The protective effects of Rhodiola crenulata extracts on Drosophila melanogaster gut immunity induced by bacteria and SDS toxicity.

The aim of this study was to observe the effect of the Rhodiola crenulata extracts on gut immunity of Drosophila melanogaster. Wild-type flies fed standard cornmeal-yeast medium were used as controls. Experimental groups were supplemented with 2.5% R. crenulata aqueous extracts in standard medium. Survival rate was determined by feeding pathogenic microorganisms and toxic compounds. The levels of reactive oxygen species and dead cells were detected by dihydroethidium and 7-amino-actinomycin D staining, respectively. The expression of antimicrobial peptides was evaluated by quantitative polymerase chain reaction, and morphological change of the intestine was imaged by an Axioskop 2 plus microscope. The results demonstrate that R. crenulata increased the survival rates of adult flies and expression of antimicrobial peptide genes after pathogen or toxic compound ingestion. Moreover, decreased levels of reactive oxygen species and epithelial cell death were associated with results in improved intestinal morphology. The pharmacological action of R. crenulata from Tibet was greater than that from Sichuan. These results indicate that the R. crenulata extracts from Tibet had better pharmacological effect on D. melanogaster gut immunity after ingestion of pathogens and toxic compounds. These results may provide the pharmacological basis for prevention of inflammatory diseases of the intestine.

Orostachys malacophylla (pall.) fisch extracts alleviate intestinal inflammation in Drosophila.

ETHNOPHARMACOLOGICAL RELEVANCE: Orostachys malacophylla (Pall.) Fisch (O. malacophylla) is a succulent herbaceous plant that is the Orostachys genus of Crassulaceae family. O. malacophylla has been widely used as a traditional Chinese medicine with antioxidant, anti-inflammatory, anti-febrile, antidote, anti-Toxoplasma gondii properties. However, the biological function of alleviating intestinal inflammation and key bioactive compounds were still unknown. AIM OF THE STUDY: We used a Drosophila model to study the protective effects and bioactive compounds of O. malacophylla water extract (OMWE) and butanol extract (OMBE) on intestinal inflammation. MATERIALS AND METHODS: Drosophila intestinal inflammation was induced by oral invasion of dextran sodium sulfate (DSS) or Erwinia carotovora carotovora 15 (Ecc15). We revealed the protective effects of two extracts by determining intestinal reactive oxygen species (ROS) and antimicrobial peptide (AMP) levels and intestinal integrity, and using network pharmacology analysis to identify bioactive compounds. RESULTS: We demonstrated that both OMWE and OMBE could ameliorate the detrimental effects of DSS, including a decreased survival rate, elevated ROS levels, increased cell death, excessive proliferation of ISCs, acid-base imbalance, and disruption of intestinal integrity. Moreover, the overabundance of lipid droplets (LDs) and AMPs by Ecc15 infection is mitigated by these extracts, thereby enhancing the flies' resistance to adverse stimuli. In addition, we used widely targeted metabolomics and network pharmacology analysis to identify bioactive compounds associated with IBD healing that are present in OMWE and OMBE. CONCLUSIONS: In summary, our research indicates that OMWE and OMBE significantly mitigate intestinal inflammation and have the potential to be effective therapeutic agents for IBD in humans.

The zinc finger protein CG12744 regulates intestinal stem cells in aged Drosophila through the EGFR and BMP pathways.

AIM: Aging is a process characterized by a time-dependent decline in the functionality of adult stem cells and is closely associated with age-related diseases. However, understanding how aging promotes disease and its underlying causes is critical for combating aging. MAIN METHODS: The offspring of UAS-Gal4 and CG12744RNAiDrosophila were cultured for 33 days to evaluate the role of CG12744 in the aging intestine. Immunofluorescence was performed to detect specific cell type markers for assessing proliferation and differentiation. qRT-PCR was used to observe the changes in signaling regulating intestinal homeostasis in the aging intestine after CG12744 knockdown. 16S rRNA-seq analysis was also conducted to elucidate the role of gut microbes in CG12744-mediated intestinal dysfunction. KEY FINDINGS: The mRNA levels of CG12744 were significantly increased in the aged midguts. Knockdown of CG12744 in progenitor cells further exacerbates the age-related intestinal hyperplasia and dysfunction. In particular, upon depletion of CG12744 in progenitors, enteroblasts (EBs) exhibited an increased propensity to differentiate along the enteroendocrine cell (EE) lineage. In contrast, the overexpression of CG12744 in progenitor cells restrained age-related gut hyperplasia in Drosophila. Moreover, CG12744 prevented age-related intestinal stem cell (ISC) overproliferation and differentiation by modulating the EGFR, JNK, and BMP pathways. In addition, the inhibition of CG12744 resulted in a significant increase in the gut microbial composition in aging flies. SIGNIFICANCE: This study established a role for the CG12744 in regulating the proliferation and differentiation of adult stem cells, thereby identifying a potential therapeutic target for diseases caused by age-related dysfunction stem cell dysfunction.

Tunable catalytic alloying eliminates stacking faults in compound semiconductor nanowires.

Planar defects in compound (III-V and II-VI) semiconductor nanowires (NWs), such as twin and stacking faults, are universally formed during the catalytic NW growth, and they detrimentally act as static disorders against coherent electron transport and light emissions. Here we report a simple synthetic route for planar-defect free II-VI NWs by tunable alloying, i.e. Cd(1-x)Zn(x)Te NWs (0 ≤ x ≤ 1). It is discovered that the eutectic alloying of Cd and Zn in Au catalysts immediately alleviates interfacial instability during the catalytic growth by the surface energy minimization and forms homogeneous zinc blende crystals as opposed to unwanted zinc blende/wurtzite mixtures. As a direct consequence of the tunable alloying, we demonstrated that intrinsic energy band gap modulation in Cd(1-x)Zn(x)Te NWs can exploit the tunable spectral and temporal responses in light detection and emission in the full visible range.

Atg2 Regulates Cellular and Humoral Immunity in Drosophila.

Autophagy is a process that promotes the lysosomal degradation of cytoplasmic proteins and is highly conserved in eukaryotic organisms. Autophagy maintains homeostasis in organisms and regulates multiple developmental processes, and autophagy disruption is related to human diseases. However, the functional roles of autophagy in mediating innate immune responses are largely unknown. In this study, we sought to understand how Atg2, an autophagy-related gene, functions in the innate immunity of Drosophila melanogaster. The results showed that a large number of melanotic nodules were produced upon inhibition of Atg2. In addition, inhibiting Atg2 suppressed the phagocytosis of latex beads, Staphylococcus aureus and Escherichia coli; the proportion of Nimrod C1 (one of the phagocytosis receptors)-positive hemocytes also decreased. Moreover, inhibiting Atg2 altered actin cytoskeleton patterns, showing longer filopodia but with decreased numbers of filopodia. The expression of AMP-encoding genes was altered by inhibiting Atg2. Drosomycin was upregulated, and the transcript levels of Attacin-A, Diptericin and Metchnikowin were decreased. Finally, the above alterations caused by the inhibition of Atg2 prevented flies from resisting invading pathogens, showing that flies with low expression of Atg2 were highly susceptible to Staphylococcus aureus and Erwinia carotovora carotovora 15 infections. In conclusion, Atg2 regulated both cellular and humoral innate immunity in Drosophila. We have identified Atg2 as a crucial regulator in mediating the homeostasis of immunity, which further established the interactions between autophagy and innate immunity.

Gbb Regulates Blood Cell Proliferation and Differentiation through JNK and EGFR Signaling Pathways in the Drosophila Lymph Gland.

The Drosophila lymph gland is an ideal model for studying hematopoiesis, and unraveling the mechanisms of Drosophila hematopoiesis can improve our understanding of the pathogenesis of human hematopoietic malignancies. Bone morphogenetic protein (BMP) signaling is involved in a variety of biological processes and is highly conserved between Drosophila and mammals. Decapentaplegic (Dpp)/BMP signaling is known to limit posterior signaling center (PSC) cell proliferation by repressing the protooncogene dmyc. However, the role of two other TGF-ß family ligands, Glass bottom boat (Gbb) and Screw (Scw), in Drosophila hematopoiesis is currently largely unknown. Here, we showed that the loss of Gbb in the cortical zone (CZ) induced lamellocyte differentiation by overactivation of the EGFR and JNK pathways and caused excessive differentiation of plasmatocytes, mainly by the hyperactivation of EGFR. Furthermore, we found that Gbb was also required for preventing the hyperproliferation of the lymph glands by inhibiting the overactivation of the Epidermal Growth Factor Receptor (EGFR) and c-Jun N-terminal Kinase (JNK) pathways. These results further advance our understanding of the roles of Gbb protein and the BMP signaling in Drosophila hematopoiesis and the regulatory relationship between the BMP, EGFR, and JNK pathways in the proliferation and differentiation of lymph gland hemocytes.

Lactation breast abscess treated with Gualou Xiaoyong decoction and painless lactation manipulation: A case report and review of literature.

BACKGROUND: Breast abscess during lactation is a severe complication of acute mastitis, which can lead to discomfort, high fever, breast fistula, sepsis, septic shock, breast damage, disease persistence and frequent hospitalization. Breast abscesses may also lead the mother to discontinue breastfeeding, thereby harming the infant's health. The predominant pathogenic bacteria are Staphylococcus aureus, Staphylococcus epidermidis and Streptococcus. The incidence of breastfeeding abscesses in breastfeeding women ranges between 4.0% and 11.0%. In cases of breast abscess, the rate of cessation of lactation is 41.0%. In instances of breast fistula, the rate of cessation of lactation is very high (66.7%). Furthermore, 50.0% of women with breast abscesses must be hospitalized and treated with intravenous antibiotics. Treatment includes antibiotics, abscess puncture and surgical incision and drainage. The patients suffer from stress, pain and easily induced breast scarring; the disease's progression is prolonged and recurrent, interfering with infant feeding. Consequently, it is crucial to discover an adequate cure. CASE SUMMARY: A 28-year-old woman with a breast abscess was treated with Gualou Xiaoyong decoction and painless breast opening manipulation 24 d after cesarean delivery. On the 2nd d of treatment, the patient's breast mass was significantly reduced, the pain was significantly reduced, and the general asthenia was improved. All conscious symptoms disappeared after 3 d, breast abscesses faded after 12 d of treatment, inflammation images disappeared after 27 d, and normal lactation images were restored. CONCLUSION: In treating breast abscesses during breastfeeding, the combination of Gualou Xiaoyong decoction and painless lactation provides a positive therapeutic impact. This disease's treatment offers the advantages of a short course of treatment, no need to discontinue breastfeeding and the ability to rapidly mitigate symptoms, which can be used as a reference in clinical practice.