Similarly, a recent study found that greater Escherichia coli inhibitory activity and higher concentrations of HBD1 in cervicovaginal lavage (CVL) were associated with an increased risk of HIV-1 acquisition , possibly due to increased mucosal inflammation.
HBD1 HBD2 Cellular Keratinocytes, kidney (primary) epithelial cells, airway epithelial cells, female Keratinocytes, reproductive tract oral epithelial cells epithelial cells, mammary epithelial cells Cellular Monocytes, Monocytes, (also reported) macrophages, macrophages, dendritic cells dendritic cells Tissuea Pancreas Trachea, lung HBD3 HBD4 Cellular (primary) keratinocytes, airway Keratinocytes, epithelial cells, oral airway epithelial cells epithelial cells Cellular (also reported) Neutrophils Lung, kidney, Tissuea Tonsil, skin uterus, testis, gastric antrum HBD5/6 References Cellular (primary) [28, 75, 128-134] Cellular (also reported) Tissuea Epididymis (a) mRNA expression was identified in tissues but cellular source was not determined.
As to their activity, it has been demonstrated that HBD1 has minimal antimicrobial activity in the presence of oxidizing conditions.
While HBD1 is constitutively expressed, HBD2 can be induced by both inflammatory stimuli and signals derived from pathogenic or probiotic bacteria, including Escherichia coli strain Nissle and certain lactobacilli [71, 72].
Colonic CD is associated with increased secretion of HBD2 but also low HBD1 levels .
In the intestine, HBD1 is partially under the control of the nuclear receptor peroxisome proliferator activated receptor [gamma] (PPAR-[gamma]), an essential mediator of intestinal homeostasis .