Abstract
The object of this study is to observe the in vivo effect of cyclo-oxygenase-2 (Cox-2) inhibitors on the humoral response after immunization of rabbits with Salmonella typhi antigen. Albino rabbits of either sex were divided into five groups of six animals each and were administered aspirin (100 mg/kg, (BD), p.o), celecoxib (30 mg/kg O.D, p.o), indomethacin (12.5 mg/kg BD, p.o) and etoricoxib (17 mg/kg O.D, p.o) for seven days starting one day prior to immunization with S. typhi antigen (0.5 ml in each thighs), respectively. The antibody titres were measured weekly for a month using Widal agglutination test. The antibody titres in the first week were augmented in all the groups. The response was more marked in treated group as compared to control group. Later on antibody titre fell markedly in the treated groups. Selective Cox-2 inhibitors administration caused higher antibody suppression in comparison to non-selective Cox inhibitors treatment. These findings support that NSAIDs and the new Cox-2-selectivedrugs have an unsuspected target, the B cell, and attenuate antibody production. Key words: Non-steroidal anti-inflammatory drugs (NSAIDS), cost, immunomodulators, antibody production.
Highlights
Prostaglandins (PGE1 and PGE2) are critical mediators of inflammation that affect both humoral and cell-mediated immune response
Among the selective Cox-2 inhibitors, etoricoxib is more potent in suppressing antibody production as compared to celecoxib, the suppression being significantly higher at day 14 (Table 1) (Figure 4)
Our study shows that Non-steroidal anti-inflammatory drugs (NSAIDS) enhance antibody production after a week of immunization, whereas during the second and third week, antibody titres are markedly low as compared to control
Summary
Prostaglandins (PGE1 and PGE2) are critical mediators of inflammation that affect both humoral and cell-mediated immune response. PGE2 enhances antibody production and promotes type 2 immune responses (Harris et al, 2002; He et al, 2002). Activated T cells express cyclo-oxygenase-2 (Cox-2) (Fedyk et al, 1996; Iniguez et al.,, 1999), an inducible enzyme that catalyzes a series of reactions to generate PGs, led us to hypothesize that human B cells express Cox-2 and synthesize PGs upon activation. This hypothesis is supported by previous findings that proinflammatory signals increased Cox-2 expression and PG production in B cells. Cox-2 is the predominant isoform contributing to high levels of PGE2 found in chronic inflammatory conditions (Fung and Kirschenbaum, 1999)
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