Acute diquat poisoning case with multiorgan failure and a literature review: A case report.

BACKGROUND: With the withdrawal of paraquat from the market, diquat is widely used, so the treatment of diquat poisoning has become one of the focuses of emergency poisoning diagnosis and treatment. CASE SUMMARY: We studied the case of a 17-year-old male patient who drank 200 mL (20 g/100 mL) of diquat solution two hours before arriving at the hospital. Despite the use of treatments such as gastric lavage, hemoperfusion, continuous hemodialysis, glucocorticoids, and organ support, the patient's condition rapidly progressed to multiorgan failure, and he died 23.5 h after admission. CONCLUSION: We summarized the clinical characteristics and treatment strategies of diquat poisoning through this case and performed a literature review to provide a basis and direction for clinical treatment.

[The role of I-A(b)/I-E expression in dendritic cells of acute lung injury mice].

OBJECTIVE: To observe the expression of I-A(b)/I-E on circulating, lung and splenic dendritic cells (DC) in acute lung injury (ALI) mice. METHODS: Twenty-four C57BL/6 mice were randomly divided into four groups: control group, ALI 6 h, ALI 12 h and ALI 24 h group. Blood, lungs and spleens were harvested after lipopolysaccharide or phosphate butter solution administration. The expression of I-A(b)/I-E on DC was assessed by flow cytometry (FCM). IL-6 level in the lung was measured by enzyme-linked immunosorbent assay (ELISA). Lung wet weight/body weight (LW/BW) was recorded to assess lung injury. Meanwhile, pathological changes were examined under optical microscope. RESULTS: (1) lipopolysaccharide-induced ALI mice resulted in a significant increase in lung LW/BW ratio. (2) Histologically, widespread alveolar wall thickening caused by edema, marked and diffuse interstitial infiltration with inflammatory cells, and severe hemorrhage in the interstitium and alveolus were observed in the ALI groups. (3) The level of IL-6 in lung tissue was significantly enhanced in ALI mice. (4) FCM analysis showed that I-A(b)/I-E expressions on lung DC [(73 ± 9)%], and splenic DC [(81 ± 8)%] were significantly higher than that on circulating DC [(24 ± 7)%;P < 0.05] in control mice. (5) In ALI mice, the expressions of I-A(b)/I-E on peripheral blood DC were (34 ± 17)% at 6 h, (51 ± 16)% at 12 h, (50 ± 17)% at 24 h respectively; I-A(b)/I-E expressions on lung DC were (82 ± 14)% at 6 h, (88 ± 6)% at 12 h, (90 ± 10)% at 24 h respectively; the expressions of I-A(b)/I-E on splenic DC were (88 ± 8)% at 6 h, (89 ± 4)% at 12 h, (93 ± 9)% at 24 h respectively, which were also significantly higher than those on the peripheral blood DC (P < 0.05). (6) The I-A(b)/I-E expressions on circulating DC in ALI mice at 12 h and 24 h was significantly higher than that on circulating DC in control mice (P < 0.05). (7) The I-A(b)/I-E expressions on lung DC and splenic DC in ALI mice at 24 h were significantly higher than those on lung DC and splenic DC in control mice (P < 0.05). (8) There was a significant correlation of I-A(b)/I-E expression on respiratory DC with the IL-6 level and lung injury score in LPS-induced ALI group (P < 0.05). CONCLUSIONS: There is a dynamic characteristic in the expression I-A(b)/I-E on circulating, lung and splenic DC populations in ALI mice. I-A(b)/I-E on pulmonary DC seems to play an important role in the pathogenesis of ALI.

Kinetic and distinct distribution of conventional dendritic cells in the early phase of lipopolysaccharide-induced acute lung injury.

Respiratory dendritic cells (DCs), especially conventional DCs (cDCs), are critically involved in the induction phase of the immune response in the respiratory system. However, little information concerning cDC kinetics in acute lung injury (ALI) is available. In this study, we have used a murine model of LPS-induced ALI to examine the kinetics and phenotype of respiratory, circulating and splenic cDCs. cDCs in the lung, blood, and spleen and the IL-6 level in the lung were detected at 6, 12 and 24 h after PBS or LPS challenge. In the ALI group, a rapid cDCs accumulation in the lung was observed, and there were highly significant correlations between the frequency of respiratory cDCs or the percentage of cDC expressing CD80 and the IL-6 concentration. However, the frequency of peripheral blood cDCs decreased rapidly in ALI mice, followed by a marked expansion. In addition, splenic cDCs only showed a transient expansion in ALI. cDCs within the blood, lungs and spleens had undergone a modest maturation in the ALI group. Our findings demonstrate that LPS-induced ALI provokes a dynamic and distinct distribution as well as phenotype changes in pulmonary, circulatory and splenic cDC populations. Lung cDCs may participate in the early inflammatory response to ALI.

Losartan inhibits conventional dendritic cell maturation and Th1 and Th17 polarization responses: Νovel mechanisms of preventive effects on lipopolysaccharide-induced acute lung injury.

Acute lung injury (ALI) remains one of major causes of morbidity and mortality in intensive care medicine. The lack of efficient pharmacological interventions contributes to the high mortality rate of ALI. Losartan, an antagonist of angiotensin II (Ang II) type 1 receptor, is a potent therapeutic drug for ALI. Recent reports suggest that losartan inhibits the maturation of dendritic cells (DCs), impairs T-helper (Th) 1 immune response and ultimately attenuates inflammation in several Ang II-mediated inflammatory diseases. However, the possible protective mechanisms of losartan in ALI remain poorly understood. This study was aimed to define the effect of losartan on the frequency and phenotype of respiratory conventional DCs (cDCs) and Th cells polarization in lipopolysaccharide (LPS)-induced ALI mice. Results demonstrate that early after induction of LPS-induced ALI, cDCs expressing modest amounts of CD80 rapidly accumulated in the lungs. In addition, polarized Th1 and Th17 responses were markedly increased in LPS-induced ALI mice at 24 and 48 h. Of note, losartan led to inhibition of respiratory cDCs maturation at 6 h and suppressed Th1 and Th17 polarization responses compared with ALI mice at 24 and 48 h. Collectively, our findings may provide a novel and, at least, partial explanation for the protective effects by which losartan inhibits lung cDCs maturation and suppresses Th1 and Th17 immune responses.