Impact of bioclimatic factors on physio-biochemical and molecular response of slow-growing poultry reared in tropics.

Most of the climatic studies projected on heat stress have considered heat extremes, but not the humidity. Hence, this work was carried out to evaluate thermotolerance, production performance, physio-biochemical and immunological response of slow-growing poultry towards various temperature-humidity levels in coastal climate. A total of 240 straight run CARI-Debendra birds were reared in three groups based on temperature-humidity indices (THI > 80, = 75-80 and < 75). Significant difference (P < 0.01) in rectal and body surface temperatures was observed among treatment groups. Lowest body weight was observed in THI > 80 group as 1.45 kg at 12 weeks. There was no significant difference in feed intake and FCR; however, total water intake had increased in heat-stressed group. Birds under THI > 80 group had significantly low gizzard weight only at the 12th week compared to other groups. Significant differences (P < 0.05) in relative weight and length of intestine were noticed which was comparable between seasonal control and THI > 80 group but lower than THI < 75 group at the 6th week. However, at the 12th week, intestinal weight varied among the groups (P = 0.08), but intestinal size did not differ. Among immune organs, significant difference (P < 0.05) was noted only in weight of thymus. Except Cl-, other biochemical indices such as cholesterol, lactate dehydrogenase, creatinine kinase, K+ and Na+ did not differ among treatment groups. Relative expression of HSP70 gene was differed significantly (P < 0.01) in the liver, intestine and breast muscles under different THI. The changes reported in seasonal control group during month of October to December revealed better thermotolerance capacity and adaptability of CARI-Debendra birds to coastal hot-humid climate. However, response of this breed to heat stress (THI > 80) reported decrease in growth, immune response and mineral balance attributable to heat loss efficacy in high humidity.

Role of nitric oxide in the regulation of immune responses during rabies virus infection in mice.

Rabies virus (RABV) stimulates nitric oxide (NO) production, which either triggers T cell differentiation or suppresses T cell function depending on its concentration. Herein, we assessed the potential role of NO in regulation of immune responses during RABV infection in mice model. The experimental animals were divided into four groups and 100LD50 of challenge virus standard (CVS) strain of RABV was inoculated intracerebrally on day 0 and subsequently aminoguanidine (AG; inducible nitric oxide synthase inhibitor) was injected intraperitoneally twice a day, up to 6 days. The samples were collected at 2, 4, 6, 8, 9, 10 and 12 days post infection (DPI). The immune cells including CD4+, CD8+ T lymphocytes and natural killer (NK) cells were estimated from peripheral blood mononuclear cells (PBMCs) and splenocytes. Serum total NO concentration, histopathology, immunohistochemistry, direct fluorescent antibody technique and TUNEL assay was performed. Infection with CVS resulted in significant early increase in CD4+, CD8+ and NK cells in blood and spleen until 2 DPI. From 4 DPI onwards significant reduction was noticed in these parameters which coincided with increased NO on 4 DPI, rising to maximum on 8 DPI, until their death on 10 DPI. Conversely, the CVS-AG treated group showed lower levels of NO and increased number of CD4+, CD8+ and NK cells. Increased number of cells in blood and spleen coincided with increased survival time, delayed development of clinical signs, reduced viral load and less apoptotic cells. NO played important role in regulation of immune responses during RABV infection. The findings of present study confirmed the role of NO and/or iNOS using iNOS inhibitor (aminoguanidine) in immune response during RABV infection, which would further help in understanding the virus immunopathogenesis with adoption of newer antiviral strategies to counter the progression of disease.