RESUMO
METHODS: We took Peripheral blood samples from adult patients over 60 years of age with a confirmed diagnosis of IPF through biopsy or clinical criteria. Plasma separation was performed, and proinflammatory cytokines were measured using CBA. This study received approval from the ethics and research committee of the Colombian Pulmonological Foundation. RESULTS: Patients with IPF exhibited an increase in cytokines such as IL-4, INFy, and IL-6 compared to healthy older adults. CONCLUSION: Inflammatory disease has been associated with the development and coexistence of multiple chronic non-communicable diseases that have a higher incidence after 65 years of age. The involvement of adaptive immunity in the pathogenesis of IPF has been described as an imbalance in the Th1/Th2 lymphocyte response. Further studies are required to identify additional markers of immunosenescence that correlate with IPF.
OBJETIVO: Identificar citoquinas proinflamatorias en el plasma de pacientes con FPI residentes en la altura de Bogotá. MÉTODOS: Se tomaron muestras de sangre periférica de pacientes adultos mayores de 60 años, con diagnóstico de FPI confirmado por biopsia o por criterios clínicos. Se realizó la separación de plasma y se midieron citoquinas proinflamatorias por CBA. Este trabajo fue aprobado por el Comité de Ética e Investigaciones de la Fundación Neumológica Colombiana. RESULTADOS: Los pacientes con FPI mostraron un aumento de citocinas como la IL-4, INFy e IL-6, en comparación con adultos mayores sanos. CONCLUSIÓN: El inflammaging ha sido asociado con el desarrollo y coexistencia de múltiples enfermedades crónicas no transmisibles que tienen mayor incidencia después de los 65 años. Se ha descrito la participación de la inmunidad adaptativa con la patogénesis de la FPI, como un desbalance en la respuesta de linfocitos Th1/Th2. Es necesario realizar más estudios que permitan identificar otros marcadores de inmunosenescencia que se correlacionen con la FPI.
Assuntos
Fibrose Pulmonar Idiopática , Humanos , Fibrose Pulmonar Idiopática/etiologia , Idoso , Masculino , Feminino , Pessoa de Meia-Idade , Inflamação , Citocinas/sangueRESUMO
The tumor immune infiltrate has an impact on cancer control and progression, additionally a growing body of evidence has proposed the role of neoadjuvant chemotherapy in modulating the contexture of the tumor immune infiltrate. Here, we performed a systematic review to evaluate the effect of chemotherapy in the immune infiltration of breast cancer tumors. We systematically searched Pubmed/MEDLINE, EMBASE, CENTRAL, and BVS databases with a cutoff date of 11/06/2022. Studies in patients with pathological diagnosis of BC, whose first line of treatment was only NAC, were included. Only published experimental studies that measured tumor immune infiltrate before and after NAC by hematoxylin and eosin (H&E) staining, immunohistochemistry (IHQ), or transcriptome were included. Reviews, studies with animal models and in-vitro models were excluded. Studies in which BC was not the primary tumor or studies with patients who received other types of neoadjuvant therapy were also excluded. The NIH quality assessment tool for before and after studies without control was used. We included 32 articles that evaluated the proximal tumor microenvironment before and after neoadjuvant chemotherapy in 2072 patients who received NAC as first line of treatment and who were evaluated for immune infiltrate in the pre- and post-chemotherapy tumor sample. Results were divided into two major categories immune cells and in-situ expression of immune checkpoints and cytokines. Qualitative synthesis was performed with the 32 articles included, and in nine of them a quantitative analysis was achieved, resulting in six meta-analyses. Despite high heterogeneity among the articles regarding treatment received, type of tumor reported, and techniques used to evaluate immune infiltrate, we found a significant decrease of TILs and FoxP3 expression after neoadjuvant chemotherapy. The study protocol was registered in PROSPERO 2021 (Protocol ID: CRD42021243784) on 6/29/2021.