Effects of inhibitors of inflammatory mediators and cytokines on eosinophil and neutrophil accumulation induced by Mycobacterium bovis bacillus Calmette-Guérinin mouse pleurisy

Abstract

In this work we characterize the Mycobacterium bovis bacillus Calmette‐Guérin(BCC) ‐induced pleurisy and investigate the role of chemical mediators and cytokines in BCG‐induced granulocyte accumulation at 24 h. Intrathoracic injection of BCG in C57B1/6 mice induces a biphasic inflammatory reaction with intense leukocyte accumulation at 24 h and 15 days. Neutrophils were observed in the pleural cavity at 4‐24 h, mononuclear cells and eosinophils after 24 h. A new wave of mononuclear cells and neutrophils were observed after 15 days. Pretreatments with dexamethasone, BW 755C, BW A4C, WEB 2170, L‐NAME, and monoclonal antibody (mAb) anti‐interleukin‐5 (IL‐5; TRFK‐5) had inhibited the eosinophil accumulation. On the other hand, only the pretreatments with dexamethasone, L‐NAME, or mAb antitumor necrosis factor a (TNF‐α; MP6‐XT3) had inhibited the neutrophil influx. These results suggest the involvement of leukotrienes, platelet‐activating factor, nitric oxide, and IL‐5 in the eosinophil accumulation, and a role for nitric oxide and TNF‐α in the neutrophil influx induced by BCG. J. Leukoc. Biol. 62: 778–785; 1997.

Proinflammatory CD4+CD45RBhi Lymphocytes Promote Mammary and Intestinal Carcinogenesis in Apc Min/+ Mice

“…TNF-a is a potent effector cytokine in the pathogenesis of IBD in humans (17) and in mice (18,19) and has been associated with poor prognosis in several human cancers, including mammary carcinoma (20). To determine whether TNF-a is critical for intestinal and mammary carcinoma seen in our model, we treated Apc Min/+ mice that received T E cells (n = 14) with anti-TNF-a neutralizing antibody (21). We find that mice that receive 200 Ag/mouse of anti-TNF-a antibody thrice weekly for 1 week had significantly (P < 0.001) fewer intestinal adenomas when compared with Apc Min/+ mice that receive sham antibody alone (n = 8; Fig.…”

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

“…In animal models of mycobacterial infection, a drastic expansion of the ␥␦ T cell population is observed in the blood and tissue sites (34 -36). In this study we used a model of pleural mycobacteria infection, which allows an evaluation of early inflammatory cell recruitment induced by infection (37,38). Within 24 h of infection, significantly increased numbers of neutrophils, eosinophils, monocytes, and lymphocytes are recovered from the pleural cavity (37,38).…”

Toll-Like Receptor-2-Mediated C-C Chemokine Receptor 3 and Eotaxin-Driven Eosinophil Influx Induced by Mycobacterium bovis BCG Pleurisy

“…Mycobacterial infections frequently show eosinophil recruitment in both naturally occurring infections in human patients (11,26) and in animal experimental infections (6,14,17,20,27). Enhanced eosinophil recruitment to sites of infection has been associated with unrestricted growth of mycobacteria observed in mouse susceptible strains in contrast to resistant ones (27) and in mice deficient in gamma interferon (IFN-␥ Ϫ/Ϫ ) that are highly susceptible to infection with tuberculosis-causing organisms (13).…”