Different Subsets of Macrophages in Patients with New Onset Tuberculous Pleural Effusion

Abstract

ObjectiveMacrophages are the infiltrate components of tuberculous pleural effusion (TPE). This study is aimed at examining the role of different subsets of macrophages in pleural fluid (PF) and peripheral blood (PB) from patients with new onset TPE.MethodsThe numbers of PB and PF CD163+, CD206+ and CD115+ macrophages in 25 patients with new onset TPE and 17 healthy controls (HC) were determined by flow cytometry. The concentrations of serum and PF cytokines were determined by cytometric bead array (CBA) and enzyme-linked immunosorbentassay (ELISA). The potential association between the numbers of different subsets of macrophages and the values of clinical measures in TPE patients were analyzed.ResultsThe numbers of PB CD14+CD163− M1-like and CD14+CD163− interleukin (IL)-12+ M1 macrophages were significantly higher than that in the HC, but lower than PF, and the numbers of PF CD14+CD163+, CD14+CD163+CD206+, CD14+CD163+CDll5+ M2-like, and CD14+CD163+IL-10+ M2 macrophages were less than PB in the TPE patients. The levels of serum IL-1, IL-6, IL-8, IL-12, tumor growth factor (TGF)-β1, and tumor necrosis factor (TNF)-α in the TPE patients were significantly higher than that in the HC, but lower than that in the PF. The levels of PF IL-10 were significantly higher than that in the PB of patients and HC. In addition, the levels of serum IL-12 and TNF-α were correlated positively with the values of erythrocyte sedimentation rate (ESR) and the numbers of ESAT-6- and culture filtrate protein 10 (CFP-10)-specific IFN-γ-secreting T cells, and the levels of PF TNF-α were correlated positively with the levels of PF adenosine deaminase (ADA) and lactate dehydrogenase (LDH) in those patients.ConclusionOur data indicate that Mycobacterium tuberculosis (M. tb) infection induces M1 predominant pro-inflammatory responses, contributing to the development of TPE in humans.

Tuberculosis is associated with expansion of a motile, permissive and immunomodulatory CD16+ monocyte population via the IL-10/STAT3 axis

“…Their final differentiation program might result as a consequence of the microenvironment shaped in health and disease pro-npg www.cell-research.com | Cell Research gression contexts. In agreement with a recent description of CD163 + macrophages during the onset of tuberculous pleurisy [70], we show that this M2-like macrophage is particularly enriched within the CD14 + CD16 + cell population isolated from the pleural cavity of TB patients. Considering that the CD16 + population expansion displays an M2-like phenotype in the pleural cavity from TB patients, and that TB pleural effusion activates STAT3 phosphorylation in monocytes from healthy donors and stimulates their protease-dependent migration, we infer that the environmental signals within Mtb infection sites perpetuate the CD16 + CD163 + MerTK + pSTAT3 + activation program and possibly also serve as chemoattractant.…”

Phenotypic Diversity and Emerging New Tools to Study Macrophage Activation in Bacterial Infectious Diseases

“…This is illustrated by the example of pleural macrophages. Tuberculous pleural effusion, an extra-pulmonary form of tuberculosis, is associated with the M1 profile in pleural fluid that is characterized by an increase in M1 macrophages and inflammatory cytokines ( 47 ).…”

Antibiotics induce polarization of pleural macrophages to M2-like phenotype in patients with tuberculous pleuritis

“…Tuberculous pleuritis is caused by delayed type hypersensitivity responses to mycobacterial antigens in the pleural space with low bacterial burden 7 . Although ~70% pleural fluid cells are T cells, pleural macrophages are also known to contribute to the pathogenesis of tuberculous pleuritis and the outcome of different clinic forms of TB 8 , 9 .…”

“…For example, in newly onset TB patients and during the early phase of M . tuberculosis infection, macrophages exhibit an M1-like phenotype producing pro-inflammatory cytokines and contributing to the development of TPE 8 .…”