Skip to main content
Figure 1 | Tobacco Induced Diseases

Figure 1

From: Cigarette smoke extract induces differential expression levels of beta-defensin peptides in human alveolar epithelial cells

Figure 1

Expression of Antimicrobial peptides A. Expression of hBD1. The constitutively expressed β-defensin, hBD1, is not induced by IL-1β treatment, as measured by qRT-PCR (Control = 1.000+/−0.324, IL-1β =1.123+/−0.086) (n = 3). Although the means differ, the treatment by cigarette smoke extract (CSE) did not statistically significantly alter the level of hBD1 expression as measured by T-test (Control = 1.000+/−0.324, CS = 0.643+/−0.046, p > 0.05). B. Expression of hBD3, hBD5, and hBD9. Cigarette Smoke Extract (CSE) induces the expression of hBD3, hBD5 and hBD9. Following treatment with CSE the expression of hBD3, hBD5 and hBD9 were all significantly (p < 0.05) induced as measured by qRT-PCR to levels similar to those achieved with IL-1β treatment. (hBD3 was 7.95 fold increased (p = 0.032), hBD5 was 2.8 fold increased (p = 0.0083) and hBD9 was 4.2 fold increased (p = 0.0078). n = 3 for hBD3, 9, n = 6 for hBD5). C. Expression of hBD 8, hBD18 and LL-37. Cigarette Smoke Extract (CSE) does NOT induce expression of hBD8, hBD18, LL-37. Measured by qRT-PCR, the expression of hBD8 and LL-37 is not significantly induced in response to cigarette smoke extract (p > 0.05), however these defensins are significantly (p < 0.05) induced by IL-1β treatment. HBD18 was also not statistically significantly induced with cigarette smoke extract, although the means differed (Control = 1.000+/−0.287, CSE = 3.207+/−1.862, p = 0.31)(n = 3).

Back to article page