Inflammatory Cell Differentiation and Chemotaxis and Extracellular Tissue Repair Markers Are Correlated with Pulmonary Dysfunction in HIV Infected Individuals Presenting with Community-Acquired Pneumonia

Ruochen Mao, Adriana Trajtman, Breanne Head, Iván Arturo Rodríguez Sabogal, Ruth Cabrera, Diana Marín, Lucelly López, Jenniffer Rodiño, Yudy Aguilar, Mariana Herrera Díaz, Lázaro Agustín Vélez, Zulma Vanessa Rueda, Yoav Keynan

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

1 Cita (Scopus)

Resumen

Prior studies have shown that HIV patients develop permanent pulmonary dysfunction following an episode of community-Acquired pneumonia (CAP). However, the mechanism causing pulmonary dysfunction remains an enigma. HIV patients experience chronic inflammation. We hypothesized that CAP exacerbates inflammation in HIV patients resulting in an accelerated decline in lung function. A prospective cohort pilot study enrolled HIV patients hospitalized in Medellin, Colombia, with a diagnosis of CAP. Sixteen patients were eligible for the study; they were split into 2 groups: HIV and HIV+CAP. Plasma, sputum, and pulmonary function test (PFT) measurements were retrieved within 48 h of hospital admission and at 1 month follow-up. The concentrations of 13 molecules and PFT values were compared between the 2 cohorts. The HIV+CAP group had lower lung function compared to the HIV group; forced vital capacity (FVC)% predicted and forced expiratory volume in 1 s (FEV1)% predicted decreased, while FEV1/FVC remained constant. APRIL, BAFF, CCL3, and TIMP-1 correlated negatively with FVC% predicted and FEV1% predicted; the relationships however were moderate in strength. Furthermore, the concentrations of BAFF, CCL3, and TIMP-1 were statistically significant between the 2 groups (P ≤ 0.05). Our results indicate that HIV patients with CAP have a different inflammatory pattern and lower lung function compared to HIV patients without CAP. BAFF, CCL3, and TIMP-1 were abnormally elevated in HIV patients with CAP. Future studies with larger cohorts are required to verify these results. In addition, further investigation is required to determine if BAFF, CCL3, and TIMP-1 play a role in the process causing pulmonary dysfunction.

Idioma originalInglés
Páginas (desde-hasta)106-115
Número de páginas10
PublicaciónJournal of Interferon and Cytokine Research
Volumen40
N.º2
DOI
EstadoPublicada - feb. 2020

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Publisher Copyright:
© Mary Ann Liebert, Inc., publishers 2020.

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