Differential Production of Chemokines and Their Role in Neutrophil Infiltration in Rat: Allergic Inflammation

Nakagawa, Hideo; Ando, Yumiko; Takano, Katsuhiko; Sunada, Y.

doi:10.1159/000023893

Cited by 17 publications

(21 citation statements)

References 12 publications

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“…From these results, it has been concluded that MIP-1α, together with CINCs, plays an important role in infiltration of neutrophils into inflammatory sites in rats. However, it has also been reported that CINCs, but not MIP-1α, play an important role in neutrophil infiltration into the site of FITC-ovalbumin-induced allergic inflammation in rats (21). The discrepancy between the models is unclear at the present time but may depend on different inflammatory stimuli.…”

Section: Discussionmentioning

confidence: 75%

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Chemokine Production by Rat Macrophages Stimulated with Streptolysin O from Streptococcus pyogenes

Mitsui

Takano

Nakatani

et al. 2002

Microbiology and Immunology

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The contribution of streptolysin O (SLO) from Streptococcus pyogenes to neutrophil infiltration in inflammatory lesions was determined by production of cytokine‐induced neutrophil chemoattractant (CINC)−1, −2 and −3, and macrophage inflammatory protein (MIP)‐1α by rat macrophages stimulated with SLO in culture. Active SLO induced the production of CINCs and MIP‐1α in dose‐ and time‐dependent manners. These inductions were ascertained by chemokine mRNA expression in macrophages. Streptolysin S was without effect. The SLO‐cholesterol complex induced the chemokine production in proportion to the residual hemolytic activity of the complex. In addition, the effects of SLO on the chemokine production were confirmed by the injection of active SLO into the preformed air pouch on the back of rats. The infiltration of neutrophils into the pouch fluid (exudate) increased steadily with a lag phase of about 2 hr. The major chemokine found in exudates was MIP‐1α but not CINCs. In this study, it became clear that active SLO, but not the inactive one, contributed to the production of MIP‐1α and CINCs in the conditioned medium and in exudates.

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Section: Discussionmentioning

confidence: 75%

“…In addition to CINCs, MIP-1α, a CC chemokine, was also purified as a neutrophil chemoattractant from conditioned medium of lipopolysaccharide (LPS)-stimulated rat macrophages (25). It has been demonstrated that CINCs and MIP-1α are potent chemoattractants for rat neutrophils in vitro and in vivo (21,23,32,37,40).…”

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confidence: 99%

Chemokine Production by Rat Macrophages Stimulated with Streptolysin O from Streptococcus pyogenes

Mitsui

Takano

Nakatani

et al. 2002

Microbiology and Immunology

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“…These cytokines are potent chemotactic factors for rat neutrophils both in vitro and in vivo and can be induced by LPS, IL-1, and TNF-␣ (Watanabe et al, 1991). Furthermore, CINCs have similar ability to induce chemotaxis and to activate rat neutrophils, suggesting that their contribution to neutrophil infiltration depends on the amount of each present in a certain inflammatory site (Nakagawa et al, 1998). Thus, our data that only CINC-3 mRNA expression is increased in lung tissue from capsaicinpretreated rats upon antigen exposure indicate a pivotal role for this cytokine in the airways neutrophil infiltration of the capsaicin neonatal model.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms Involved in the Enhancement of Allergic Airways Neutrophil Influx by Permanent C-Fiber Degeneration in Rats

Franco‐Penteado¹,

DeSouza²,

Camargo³

et al. 2004

J Pharmacol Exp Ther

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This study was undertaken to clarify the mechanisms by which C-fiber degeneration at neonatal stages exacerbates the inflammatory responses of rat airways. Rats were treated with capsaicin at neonatal stages and immunized with ovalbumin (OVA) at adult ages. Challenge of capsaicin-pretreated rats with OVA promoted a higher influx of neutrophils in bronchoalveolar lavage (BAL) fluid compared with the vehicle group. No significant differences were found for the other cell types. The increased adhesion of N-formyl-methionyl-leucyl-phenylalanine (fMLP; 0.1 M)-and phorbol myristate acetate (PMA; 1 M)-treated neutrophils to fibronectin-coated wells did not differ among vehicle-and capsaicin-pretreated rats. Additionally, fMLP (10 M), platelet-activating factor (0

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“…When the i.t. addition of a potent neutrophil chemokine, CINC-1 (a member of the IL-8 family), in combination with OVA was examined in terms of its ability to induce an LAR, CINC-1 (up to 100-fold more than C5a desArg) was incapable of LAR induction when used in combination with the Ag, thus suggesting that C5a plays a specific role in the LAR in this model (36). Nevertheless, CINC-1 plus OVA stimulation resulted in the accumulation of as many granulocytes in the bronchial submucosa as were noted with C5a desArg plus OVA.…”

Section: Discussionmentioning

confidence: 99%

Contribution of Anaphylatoxin C5a to Late Airway Responses After Repeated Exposure of Antigen to Allergic Rats

Abe¹,

Shibata

Akatsu

et al. 2001

The Journal of Immunology

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We attempted to elucidate the contribution of complement to allergic asthma. Rat sensitized to OVA received repeated intratracheal exposures to OVA for up to 3 consecutive days, and pulmonary resistance was then estimated for up to 6 h after the last exposure. Whereas the immediate airway response (IAR) in terms of RL tended to decrease in proportion to the number of OVA exposures, late airway response (LAR) became prominent only after three. Although premedication with two kinds of complement inhibitors, soluble complement receptor type 1 (sCR1) or nafamostat mesylate, resulted in inhibition of the IAR after either a single or a double exposure, the LAR was inhibited after the triple. Premedication with a C5a receptor antagonist (C5aRA) before every exposure to OVA also inhibited the LAR after three. Repeated OVA exposure resulted in eosinophil and neutrophil infiltration into the bronchial submucosa which was suppressed by premedication with sCR1 or C5aRA. Up-regulation of C5aR mRNA was shown in lungs after triple OVA exposure, but almost no up-regulation of C3aR. Pretreatment with sCR1 or C5aRA suppressed the up-regulation of C5aR expression as well as cytokine messages in the lungs. The suppression of LAR by pretreatment with sCR1 was reversed by intratracheal instillation of rat C5a desArg the action of which was inhibited by C5aRA. In contrast, rat C3a desArg or cytokine-induced neutrophil chemoattractant-1 induced cellular infiltration into the bronchial submucosa by costimulation with OVA, but these had no influence on the LAR. These differences might be explained by the fact that costimulation with OVA and C5a synergistically potentiated IAR, whereas that with OVA and either C3a or cytokine-induced neutrophil chemoattractant-1 did not. C5a generated by Ag-Ab complexes helps in the production of cytokines and contributes to the LAR after repeated exposure to Ag.

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Differential Production of Chemokines and Their Role in Neutrophil Infiltration in Rat: Allergic Inflammation

Cited by 17 publications

References 12 publications

Chemokine Production by Rat Macrophages Stimulated with Streptolysin O from Streptococcus pyogenes

Chemokine Production by Rat Macrophages Stimulated with Streptolysin O from Streptococcus pyogenes

Mechanisms Involved in the Enhancement of Allergic Airways Neutrophil Influx by Permanent C-Fiber Degeneration in Rats

Contribution of Anaphylatoxin C5a to Late Airway Responses After Repeated Exposure of Antigen to Allergic Rats

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