Search

Influenza is a major cause of respiratory tract infection. Although most cases do not require further hospitalization, influenza periodically causes epidemics in humans that can potentially infect and kill millions of people. To countermeasure this threat, new vaccines need to be developed annually to match emerging influenza viral strains with increased resistance to existing vaccines. Thus, there is a need for finding and developing new anti-influenza viral agents as alternatives to current treatments. Here, we tested the antiviral effects of an extract from the stems and roots of Salacia reticulata (SSRE), a plant rich in phytochemicals such as salacinol, kotalanol and catechins, on H1N1 influenza virus-infected mice. Following oral administration of 0.6 mg/day of SSRE, the incidence of coughing decreased in 80% of mice, and only one case of severe pulmonary inflammation was detected. Moreover, when compared with mice given Lactobacillus casei JCM1134, a strain previously shown to help increase in vitro NK cell activity, SSRE-administered mice showed greater and equal NK cell activity in splenocytes and pulmonary cells, respectively, at high effector cell:target cell ratios. Next, to test whether or not SSRE would exert protective effects against influenza in the absence of gut microbiota, mice were given antibiotics before being inoculated influenza virus and subsequently administered SSRE. SSRE administration induced an increase in NK cell activity in splenocytes and pulmonary cells at levels similar to those detected in mice not treated with antibiotics. Based on our results, it can be concluded that phytochemicals in the SSRE exerted protective effects against influenza infection putatively via modulation of the immune response including enhancement of NK cell activity, although some protective effects were not necessarily through modulation of gut microbiota. Further investigation is necessary to elucidate the molecular mechanisms underlying the protective effects of SSRE against influenza infection.

Transcriptome analyses were conducted on the ileal mucosa of 14-35 day-old piglets to investigate postnatal gut development during suckling and post-weaning. The transcriptome profiles of 14 day-old suckling piglets showed a considerably higher number of differentially expressed genes than did those of 21, 28 and 35 day olds, indicating an intensive gut development during the first 14-21 postnatal days. In addition, the analysis of biological pathways indicated that Chemotaxis Leucocyte chemotaxis was the most significantly affected pathway in suckling piglets between 14 and 21 days of age. Weaning negatively affected pathways associated with acquired immunity, but positively affected those associated with innate immunity. Interestingly, pathway Chemotaxis Leucocyte chemotaxis was found positively affected when comparing 14 and 21 day-old suckling piglets, but negatively affected in 28 day-old piglets weaned at 21 days of age, when compared with 28 day-old suckling piglets. Genes CXCL13, SLA-DOA (MHC class II), ICAM1, VAV1 and VCAM1 were involved in the pathway Chemotaxis Leukocyte chemotaxis and they were found to significantly change between 14 and 21 day-old suckling piglets, and between groups of suckling and weaned piglets. The expression of these genes significantly declined after weaning at 14, 21 and 28 days of age. This decline indicated that CXCL13, SLA-DOA, ICAM1, VAV1 and VCAM1 may be involved in the development of Peyer’s patches because lower gene expression clearly corresponded with smaller areas of Peyer’s patches in the ileal mucosa of piglets. Moreover, weaning piglets prior to a period of intensive gut development i.e., 14 days of age, caused significant adverse effects on the size of Peyer’s patches, which were not reverted even 14 days post-weaning.