A role for lymphocytes and cytokines on the eosinophil migration induced by LPS

Castro‐Faria‐Neto, Hugo C.; Penido, Carmen; Larangeira, Andréia P; Silva, Adriana Ribeiro; Bozza, Patrı́cia T.

doi:10.1590/s0074-02761997000800026

Cited by 6 publications

(3 citation statements)

References 19 publications

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“…Our results show a significant increase in the number of γδ T lymphocytes expressing intracellular CCL11, but only a slight increase of IL-5 and IL-4. However, γδ T lymphocytes may be indirectly modulating the production of IL-5 and IL-4 by other cell populations, such as pleural macrophages, αβ T lymphocytes and endothelial cells, in a cross-talk previously demonstrated to occur in LPS-induced pleurisy [54,55] and other reactions [2,14].…”

Section: Discussionmentioning

confidence: 99%

Requirement of L-selectin for γδ T lymphocyte activation and migration during allergic pleurisy: Co-relation with eosinophil accumulation

Costa

Nihei

Mengel

et al. 2009

International Immunopharmacology

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Section: Discussionmentioning

confidence: 99%

Requirement of L-selectin for γδ T lymphocyte activation and migration during allergic pleurisy: Co-relation with eosinophil accumulation

Costa

Nihei

Mengel

et al. 2009

International Immunopharmacology

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“…1A). The recruitment of monocytes, neutrophils, and eosinophils to the pleural cavity induced by LPS occurs through indirect mechanisms via the release of inflammatory mediators and is sensitive to glucocorticoid treatment (18,19). Likewise, Fig.…”

Section: Chemokine Neutralization By Vckbp Inhibits Lps-induced ␥␦mentioning

confidence: 99%

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

Penido

Vieira‐de‐Abreu

Bozza

et al. 2003

The Journal of Immunology

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γδ T lymphocytes are involved in a great variety of inflammatory and infectious responses. However, the mechanisms by which γδ T lymphocytes migrate to inflamed sites are poorly understood. In this study we investigate the role of monocyte chemotactic protein (MCP)-1 in regulating γδ T cell migration after LPS or Mycobacterium bovis bacille Calmette-Guérin (BCG) challenge. LPS-induced γδ T cell influx was significantly inhibited by either pretreatment with dexamethasone or vaccinia virus Lister 35-kDa chemokine binding protein, vCKBP, a CC chemokine neutralizing protein, suggesting a role for CC chemokines in this phenomenon. LPS stimulation increased the expression of MCP-1 mRNA and protein at the inflammation site within 6 h. It is noteworthy that LPS was unable to increase MCP-1 production or γδ T cell recruitment in C3H/HeJ, indicative of the involvement of Toll-like receptor 4. γδ T cells express MCP-1 receptor CCR2. Pretreatment with anti-MCP-1 mAb drastically inhibited LPS-induced in vivo γδ T cell mobilization. Indeed, MCP-1 knockout mice were unable to recruit γδ T cells to the pleural cavity after LPS stimulation, effect that could be restored by coadministration of MCP-1. In addition, BCG-induced γδ lymphocyte accumulation was significantly reduced in MCP-1 knockout mice when compared with wild-type mice. In conclusion, our results indicate that LPS-induced γδ T lymphocyte migration is dependent on Toll-like receptor 4 and sensitive to both dexamethasone and CC chemokine-binding protein inhibition. Moreover, by using MCP-1 neutralizing Abs and genetically deficient mice we show that LPS- and BCG-induced γδ T lymphocyte influx to the pleural cavity of mice is mainly orchestrated by the CC chemokine MCP-1.

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“…Neutrophils and eosinophils are activated following chemotherapy and are thought to contribute to the Mazzoti reaction (59,60). Interestingly, in addition to neutrophils, eosinophils are also recruited to tissues following exposure to LPS (61).…”

Section: The Influence Of Wolbachia Inflammatory Mediators On Other Cmentioning

confidence: 99%

Wolbachiabacteria in filarial immunity and disease

Taylor

Cross

Ford

et al. 2001

Parasite Immunology

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Lymphatic filarial nematodes are infected with endosymbiotic Wolbachia bacteria. Lipopolysaccharide from these bacteria is the major activator of innate inflammatory responses induced directly by the parasite. Here, we propose a mechanism by which Wolbachia initiates acute inflammatory responses associated with death of parasites, leading to acute filarial lymphangitis and adverse reactions to antifilarial chemotherapy. We also speculate that repeated exposure to acute inflammatory responses and the chronic release of bacteria, results in damage to infected lymphatics and desensitization of the innate immune system. These events will result in an increased susceptibility to opportunistic infections, which cause acute dermatolymphangitis associated with lymphoedema and elephantiasis. The recognition of the contribution of endosymbiotic bacteria to filarial disease could be exploited for clinical intervention by the targeting of bacteria with antibiotics in an attempt to reduce the development of filarial pathology.

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A role for lymphocytes and cytokines on the eosinophil migration induced by LPS

Cited by 6 publications

References 19 publications

Requirement of L-selectin for γδ T lymphocyte activation and migration during allergic pleurisy: Co-relation with eosinophil accumulation

Requirement of L-selectin for γδ T lymphocyte activation and migration during allergic pleurisy: Co-relation with eosinophil accumulation

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

Wolbachiabacteria in filarial immunity and disease

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