Sex Hormones and Bacterial Infections

Léone, Marc; Textoris, Julien; Capo, Christian; Mège, Jean‐Louis

doi:10.5772/26871

Cited by 11 publications

(8 citation statements)

References 86 publications

(101 reference statements)

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“…Many host immune cells express androgen-receptor [35,36], and it is possible that C. scindens affects immune function through generation of androgens. Androgens directly affect bacterial growth and virulence [37][38][39]. Intriguingly, steroids have been shown to influence C. difficile germination [40].…”

Section: Discussionmentioning

confidence: 99%

The desA and desB genes from Clostridium scindens ATCC 35704 encode steroid-17,20-desmolase

Devendran

Mythen

Ridlon

2018

Journal of Lipid Research

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Clostridium scindens is a gut microbe capable of removing the side-chain of cortisol, forming 11β-hydroxyandrostenedione. A cortisol-inducible operon (desABCD) was previously identified in C. scindens ATCC 35704 by RNA-Seq. The desC gene was shown to encode a cortisol 20α-hydroxysteroid dehydrogenase (20α-HSDH). The desD encodes a protein annotated as a member of the major facilitator family, predicted to function as a cortisol transporter. The desA and desB genes are annotated as Nterminal and C-terminal transketolases, respectively. We hypothesized that the DesAB forms a complex and has steroid-17,20-desmolase activity. We cloned the desA and desB genes from C. scindens ATCC 35704 in pETDuet for overexpression in E.coli. The purified recombinant DesAB was determined to be a 142 ± 5.4 kDa heterotetramer. We developed an enzyme-linked continuous spectrophotometric assay to quantify steroid-17,20-desmolase. This was achieved by coupling DesAB-dependent formation of 11β-hydroxyandrostenedione with the NADPH-dependent reduction of the steroid 17-keto group by a recombinant 17β-HSDH from the filamentous fungus, Cochliobolus lunatus. The pH optimum for the coupled assay was 7.0 and kinetic constants using cortisol as substrate were K m of 4.96 ± 0.57 µM and k cat of 0.87 ± 0.076 min -1 . Substrate-specificity studies revealed that rDesAB recognized substrates regardless of 11β-hydroxylation, but had an absolute requirement for 17,21-dihydroxy 20-ketosteroids.

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Section: Discussionmentioning

confidence: 99%

The desA and desB genes from Clostridium scindens ATCC 35704 encode steroid-17,20-desmolase

Devendran

Mythen

Ridlon

2018

Journal of Lipid Research

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“…One particular NTM-associated bronchiectasis phenotype coined Lady Windermere’s syndrome is typically found in white, lean and tall women [ 80 ]. The recognised sex-related differences in microbial colonisation, infection and virulence can, at least in part, be attributed to differences in host immune response and bacterial pathogenicity; features influenced and regulated by sex steroid hormones [ 81 , 82 ].…”

Section: Gender Differences In Cf and Non-cf Bronchiectasismentioning

confidence: 99%

Gender differences in bronchiectasis: a real issue?

Vidaillac

Yong

Jaggi

et al. 2018

Breathe

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Gender differences in chronic respiratory disease, including cystic fibrosis and non-cystic fibrosis bronchiectasis are clinically apparent and of increasing importance. Differences in disease prevalence, severity and outcome are all described, however, the precise cause of the gender dichotomy and their associated underlying mechanisms have been poorly characterised. A lack of dedicated clinical and epidemiological research focused in this area has led to a paucity of data and therefore a lack of understanding of its key drivers. Diagnosis, disease pathogenesis and treatment response are all complex but important aspects of bronchiectasis with an evident gender bias. Broadening our understanding of the interplay between microbiology, host physiology and the environment in the context of chronic lung diseases, such as bronchiectasis, is critical to unravelling mechanisms driving the observed gender differences. In this review, epidemiological, biological and environmental evidence related to gender in bronchiectasis is summarised. This illustrates gender differences as a “real issue” with the objective of mapping out a future framework upon which a gender-tailored medical approach may be incorporated into the diagnosis, monitoring and treatment of bronchiectasis.Key pointsCF and non-CF bronchiectasis are complex, multifactorial chronic pulmonary diseases with gender-specific differences in their prevalence, clinical presentation and disease severity.Microbiology and host physiology (immune and inflammatory responses) are essential aspects of bronchiectasis that are influenced by gender.Sex steroid hormones vary in type, fluctuating pattern and concentration throughout life and between the genders with a potential central role in bronchiectasis-related gender differences.Gender-focused clinical and/or therapeutic intervention has the potential to narrow the observed gender gap occurring in bronchiectasis-related lung disease.Educational aimsTo summarise the existing knowledge base of gender-related differences in CF and non-CF bronchiectasis.To highlight key areas of importance in the diagnosis, monitoring and treatment of bronchiectasis that is amenable to clinical and/or pharmacological intervention to narrow the existing “gender gap”.

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“…Experimental models of infection in castrated animals with or without hormonal substitution have been used to study the role of sex hormones in bacterial infections [43]. …”

Section: Effects Of Sex Steroid Hormones On Bacterial Infectionsmentioning

confidence: 99%

Role of Sex Steroid Hormones in Bacterial-Host Interactions

García-Gómez

González‐Pedrajo

Camacho‐Arroyo

2013

BioMed Research International

168

137

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Sex steroid hormones play important physiological roles in reproductive and nonreproductive tissues, including immune cells. These hormones exert their functions by binding to either specific intracellular receptors that act as ligand-dependent transcription factors or membrane receptors that stimulate several signal transduction pathways. The elevated susceptibility of males to bacterial infections can be related to the usually lower immune responses presented in males as compared to females. This dimorphic sex difference is mainly due to the differential modulation of the immune system by sex steroid hormones through the control of proinflammatory and anti-inflammatory cytokines expression, as well as Toll-like receptors (TLRs) expression and antibody production. Besides, sex hormones can also affect the metabolism, growth, or virulence of pathogenic bacteria. In turn, pathogenic, microbiota, and environmental bacteria are able to metabolize and degrade steroid hormones and their related compounds. All these data suggest that sex steroid hormones play a key role in the modulation of bacterial-host interactions.

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Sex Hormones and Bacterial Infections

Cited by 11 publications

References 86 publications

The desA and desB genes from Clostridium scindens ATCC 35704 encode steroid-17,20-desmolase

The desA and desB genes from Clostridium scindens ATCC 35704 encode steroid-17,20-desmolase

Gender differences in bronchiectasis: a real issue?

Role of Sex Steroid Hormones in Bacterial-Host Interactions

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