CRH promotes S. pneumoniae growth in vitro and increases lung carriage in mice

Abstract

Streptococcus pneumoniae (S. pneumoniae), a commensal across the nasal passages, is responsible for the majority of infectious pneumonia cases worldwide. Previous studies have shown that hormonal factors may be influential in regulating S. pneumoniae’s transition from a non-pathogen to a pathogenic state. The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae. Mice were infected with CRH-treated S. pneumoniae via intranasal route, showing an increase in pulmonary bacterial burden. We also quantified S. pneumoniae’s response to CRH through limited serial dilutions and growth curve analysis. We demonstrated that CRH promotes S. pneumoniae titer-dependent proliferation, as well as accelerates log-phase growth. Results also showed an increase in pneumococcal-associated virulence protein A virulence gene expression in response to CRH. These results demonstrate a role for CRH in S. pneumoniae pathogenicity, thus implicating CRH in mediating the transition of S. pneumoniae into a pathogenic state.

CRH Affects the Phenotypic Expression of Sepsis-Associated Virulence Factors by Streptococcus pneumoniae Serotype 1 In vitro

“…Little is known however, regarding a bacterial species' response to CRH and other neuroendocrine factors as determinants of its virulence and pathogenicity. In previous studies, we were the first to demonstrate, to our knowledge, that CRH could directly impact S. pneumoniae's growth and in vivo pathogenesis (Ndjom and Jones, 2015 ). The results of the current study indicate that CRH potentiates morphological, genetic and functional properties vital to S. pneumoniae's virulence.…”

“…We also found that pre-exposing S. pneumoniae to CRH increased bacterial counts in the lung. Furthermore, direct exposure to CRH resulted in increased bacterial growth, and Pneumococcal-associated virulence factor A (pavA) gene expression (Ndjom and Jones, 2015 ). Collectively these results suggest a possible correlation between a bacterial pathogen's response to stress hormones (e.g., glucocorticoids) and the risk for developing sepsis and septic shock.…”

Mammalian Neuropeptides as Modulators of Microbial Infections: Their Dual Role in Defense versus Virulence and Pathogenesis

“…Proteolytic degradation of neuropeptides by microbial proteases, however, seems to be a different and more likely matter. The findings that various bacteria such as P. aeruginosa , E. faecalis , Proteus mirabilis , S. enterica , S. pyogenes , Burkholderia cenocepacia , Vibrio cholera and pathogenic yeasts such as C. albicans can cleave pivotal antimicrobial peptides including LL-37 appear to support this notion [ 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 …”

Auction market placement and a rest stop during transportation affect the respiratory bacterial microbiota of beef cattle

“…Interestingly, neurochemicals secreted during stressful events can potentially influence the composition of the respiratory tract microbiota, as these neurochemicals can interact with bacterial pathogens, modifying their growth and expression of virulence-related factors ( Lyte, 2014 ). Corticotropin-releasing hormone, a peptide hormone involved in the stress response, enhanced growth and virulence of the human respiratory pathogen Streptococcus pneumoniae , and is thought to be involved in its transition from a non-pathogenic to a pathogenic state ( Ndjom and Jones, 2015 ). In cattle, the abundance of M. haemolytica was markedly increased in recently weaned calves that were transported > 1,600 km ( Frank and Smith, 1983 ), perhaps also suggesting that the microbiota of the bovine respiratory tract respond to stress factors.…”