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

Ndjom CG, Jones HP - Front Microbiol (2015)

Bottom Line: The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Fort Worth, TX USA ; Center for Biotechnology Education, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD USA.

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.

No MeSH data available.


Related in: MedlinePlus

Corticotropin-releasing hormone (CRH)-treated Streptococcus pneumoniae increases mice lung carriage. We assessed whether or not exposing mice to S. pneumoniae (105 cells), previously treated or untreated with CRH, would result in bacterial burden for the mice. Mice (N = 5) treated with previously exposed to CRH bacteria (2.0 × 105 cells) showed an increase in lung carriage compared to the unexposed group. Bar graphs represent the mean ± SE of (N = 5) the number of CFUs in lungs. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.
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Figure 1: Corticotropin-releasing hormone (CRH)-treated Streptococcus pneumoniae increases mice lung carriage. We assessed whether or not exposing mice to S. pneumoniae (105 cells), previously treated or untreated with CRH, would result in bacterial burden for the mice. Mice (N = 5) treated with previously exposed to CRH bacteria (2.0 × 105 cells) showed an increase in lung carriage compared to the unexposed group. Bar graphs represent the mean ± SE of (N = 5) the number of CFUs in lungs. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.

Mentions: We determined whether exposing S. pneumoniae to CRH would impact its propensity to induce pulmonary infection. S. pneumoniae cultures were exposed to CRH (2.1 × 10-4mM/μl) and used for nasal infection. Bacterial colonization in the lungs of mice was significantly higher (P ≤ 0.05) in mice exposed CRH-treated S. pneumoniae (CRH-Sp) compared to untreated S. pneumoniae (Sp; Figure 1).


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

Ndjom CG, Jones HP - Front Microbiol (2015)

Corticotropin-releasing hormone (CRH)-treated Streptococcus pneumoniae increases mice lung carriage. We assessed whether or not exposing mice to S. pneumoniae (105 cells), previously treated or untreated with CRH, would result in bacterial burden for the mice. Mice (N = 5) treated with previously exposed to CRH bacteria (2.0 × 105 cells) showed an increase in lung carriage compared to the unexposed group. Bar graphs represent the mean ± SE of (N = 5) the number of CFUs in lungs. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4389549&req=5

Figure 1: Corticotropin-releasing hormone (CRH)-treated Streptococcus pneumoniae increases mice lung carriage. We assessed whether or not exposing mice to S. pneumoniae (105 cells), previously treated or untreated with CRH, would result in bacterial burden for the mice. Mice (N = 5) treated with previously exposed to CRH bacteria (2.0 × 105 cells) showed an increase in lung carriage compared to the unexposed group. Bar graphs represent the mean ± SE of (N = 5) the number of CFUs in lungs. Asterisks (∗) indicate significant (P ≤ 0.05) differences between experimental groups.
Mentions: We determined whether exposing S. pneumoniae to CRH would impact its propensity to induce pulmonary infection. S. pneumoniae cultures were exposed to CRH (2.1 × 10-4mM/μl) and used for nasal infection. Bacterial colonization in the lungs of mice was significantly higher (P ≤ 0.05) in mice exposed CRH-treated S. pneumoniae (CRH-Sp) compared to untreated S. pneumoniae (Sp; Figure 1).

Bottom Line: The current study investigated the effects of corticotropin-releasing hormone (CRH), a peptide hormone involved in stress, on the pathogenicity of S. pneumoniae.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Medical Genetics, University of North Texas Health Science Center, Fort Worth, TX USA ; Center for Biotechnology Education, Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD USA.

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.

No MeSH data available.


Related in: MedlinePlus