Role of lymphocytes in the course of murine zymosan-induced peritonitis

Kołaczkowska, Elżbieta; Barteczko, M.; Płytycz, Barbara; Arnold, Bernd

doi:10.1007/s00011-007-7131-1

Cited by 39 publications

(40 citation statements)

References 37 publications

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“…Recent work by Kolaczkowska et al [13] demonstrated comparable changes between RAG-deficient mice and wild-type mice in vascular permeability and PMN infiltration in the model of zymosan peritonitis. In contrast, work by Rajakaria et al [6] suggested that RAG-deficient mice exhibited an exaggerated peritoneal response to zymosan with increased PMN infiltration accompanied by increased TNF-α and reduced IL-10 levels.…”

Section: Lymphocytesmentioning

confidence: 99%

Regulation of Experimental Peritonitis: A Complex Orchestration

Laurin

Brissette

Lepage

et al. 2012

Nephron Exp Nephrol

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Experimental peritonitis is a frequently used inflammatory model to evaluate leukocyte recruitment. By the intrinsic characteristics of the peritoneal cavity, the various resident cell populations have a role to play in the initiation, the modulation and the resolution of peritoneal inflammation. Through various manipulations of these cell populations, we gained important knowledge on their respective roles in peritoneal inflammation. In this brief review, we will focus on the cellular regulation of leukocyte recruitment in experimental peritonitis.

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Section: Lymphocytesmentioning

confidence: 99%

Regulation of Experimental Peritonitis: A Complex Orchestration

Laurin

Brissette

Lepage

et al. 2012

Nephron Exp Nephrol

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show abstract

“…The viewpoints on the control of innate immune cells by the adaptive immune system during sepsis remain controversial (14)(15)(16)(17)(18). Research using mouse models of sepsis induced by cecal ligation and puncture (CLP) (19) produced different conclusions.…”

Section: Discussionmentioning

confidence: 99%

“…van Schaik et al (14) showed that T cell-deficient mice exhibit markedly decreased disease severity compared to wild-type mice after E. coli injection and suggested that T cells may stimulate innate immune responses, resulting in enhancement of disease. The research on BALB/c mice and Rag-deficient mice with peritonitis induced by zymosan showed that lymphocytes do not have a significant impact on zymosan peritonitis in mice (16). Kim et al (9) showed that lymphocytes suppress activation of innate immune cells in Rag-1 knockout mice with poly (I: C)-induced SIRS.…”

Section: Discussionmentioning

confidence: 99%

Mitogen-activated protein kinase phosphatase-1 expression in macrophages is controlled by lymphocytes during macrophage activation

Luo

Yang

Yao³

et al. 2011

Int J Mol Med

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Abstract. The viewpoints on the control of innate immune cells by the adaptive immune system during sepsis remain controversial. Mitogen-activated protein kinase phosphatase-1 (MKP-1) is essential to the negative control of innate immunity and suppresses the activation of macrophages by inhibiting activated mitogen-activated protein kinase (MAPK). The purpose of the current study was to observe inflammatory response and macrophage activation in mice with severe combined immunodeficiency (SCID) with endotoxemia and to determine the role of MKP-1 in the control of macrophage activation by the adaptive immune system. Endotoxemia was induced in wild-type and SCID mice by an intraperitoneal injection of lipopolysaccharide (LPS), and all of the SCID mice died. SCID mice produced more inflammatory cytokines than BALB/c mice systemically and locally. TNF-α mRNA expression was higher and MKP-1 mRNA expression was lower in peritoneal macrophages (PMa) from SCID mice compared to PMa from wild-type mice after and even before LPS injection. Thioglycollate-stimulated PMa from wild-type mice were stimulated with LPS in vitro in the presence or absence of pan-T cells. The levels of TNF-α and IL-6 were higher in the supernatants from PMa cultured alone compared to PMa co-cultured with pan-T cells, and PMa MKP-1 mRNA and protein expression were higher when PMa were co-cultured with pan-T cells. Therefore, pan-T cells can up-regulate MKP-1 expression in macrophages and inhibit the secretion of inflammatory cytokines secretion by macrophages. In SCID mice, lymphocyte deficiency, especially T cell deficiency, causes insufficient MKP-1 expression in macrophages, which can be responsible for the severe inflammation and bad prognosis of septic SCID mice. MKP-1 plays an important role in the control of macrophage activation by the adaptive immune system.

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“…Studies have shown reduced leukocyte recruitment (either PMN or M/) [11][12][13], increased leukocyte recruitment [7] or no difference [6,9,14] in various lymphocyte-deficient animals compared to control mice. It should be noted, however, that previous studies of the inflammatory responses of lymphocyte-deficient strains have not examined the numbers of circulating PMNs or monocytes or, in the case of studies of peritoneal inflammation, the numbers of resident peritoneal cells and this complicates interpretation of the available data [7,13,14].…”

Section: Discussionmentioning

confidence: 99%

“…Recent work by Kolaczkowska et al [6] demonstrated comparable changes between RAGdeficient mice and wild-type mice in vascular permeability and PMN infiltration in the model of zymosan peritonitis at the 30 min and 6 h time points, respectively [6]. In contrast, work by Rajakaria et al [7] demonstrated that RAG-deficient mice exhibited an exaggerated peritoneal response to zymosan with increased PMN infiltration evident at 2 and 6 h accompanied by increased TNF-a and reduced IL-10 levels.…”

Section: Introductionmentioning

confidence: 86%