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Staphylococcal infections and infertility: mechanisms and management

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Abstract

Infertility is a subject of worldwide concern as it affects approximately 15% of couples. Among the prime contributors of infertility, urogenital bacterial infections have lately gained much clinical importance. Staphylococcal species are commensal bacteria and major human pathogens mediating an array of reproductive tract infections. Emerging evidences are ‘bit by bit’ revealing the mechanisms by which Staphylococci strategically disrupt normal reproductive functions. Staphylococcal species can directly or through hematogenous routes can invade the reproductive tissues. In the testicular cells, epididymis as well as in various compartments of female reproductive tracts, the pathogen recognition receptors, toll-like receptors (TLRs), can recognize the pathogen-associated molecular patterns on the Staphylococci and thereby activate inflammatory signalling pathways. These elicit pro-inflammatory mediators trigger other immune cells to infiltrate and release further inflammatory agents and reactive oxygen species (ROS). Adaptive immune responses may intensify the inflammation-induced reproductive tissue damage, particularly via activation of T-helper (Th) cells, Th1 and Th17 by the innate components or by staphylococcal exotoxins. Staphylococcal surface factors binding with sperm membrane proteins can directly impair sperm functions. Although Staphylococci, being one of the most virulent bacterial species, are major contributors in infection-induced infertility in both males and females, the mechanisms of their operations remain under-discussed. The present review aims to provide a comprehensive perception of the possible mechanisms of staphylococcal infection-induced male and female infertility and aid potential interventions to address the lack of competent therapeutic measures for staphylococcal infection-induced infertility.

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Abbreviations

BV:

Bacterial vaginosis

CNS:

Coagulase-negative staphylococci

E. coli:

Escherichia coli

GnRH:

Gonadotropin releasing hormone

IFN:

Interferon

IL:

Interleukin

IRAK:

Interleukin-1 receptor-associated kinase

LH:

Luteinizing hormone

LIF:

Leukaemia inhibitory factor

LPG:

Lysyl-phosphatidyl glycerol

LTA:

Lipoteichoic acid

MAPK:

Mitogen-activated protein kinase

MHC:

Major histocompatibility complex

MPF:

Mitosis-promoting factor

MRSA:

Methicillin-resistant Staphylococcus aureus

MSSA:

Methicillin-susceptible Staphylococcus aureus

MyD88:

Myeloid differentiation primary response 88

NET:

Neutrophil extracellular trap

N. gonorrhoeae:

Neisseria gonorrhoeae

NF-kB:

Nuclear factor kappa-B

NK:

Natural killer

PBP:

Penicillin-binding protein

PID:

Pelvic inflammatory diseases

Sags:

Staphylococcal antigens

SAB:

Staphylococcus aureus bacteraemia

SAF:

Sperm-agglutinating factor

S. aureus :

Staphylococcus aureus

SEA:

Staphylococcal Enterotoxin-A

S. epidermidis :

Staphylococcus epidermidis

S. haemolyticus :

Staphylococcus haemolyticus

SIF:

Sperm immobilization factor

S. saprophyticus :

Staphylococcus saprophyticus

STD:

Sexually transmitted disease

STI:

Sexually transmitted infections

TIRAP:

Toll/interleukin-1 receptor domain-containing adapter protein

TLR:

Toll-like receptor

TNF:

Tumour necrosis factor

TSST:

Toxic shock syndrome toxin

T. vaginalis :

Trichomonas vaginalis

VISA:

Vancomycin-intermediate S. aureus

VRSA:

Vancomycin-resistant S. aureus

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The present research is funded by MAHSA University Research Grant (RP167-05/19).

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Correspondence to Sulagna Dutta or Pallav Sengupta.

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Dutta, S., Sengupta, P., Izuka, E. et al. Staphylococcal infections and infertility: mechanisms and management. Mol Cell Biochem 474, 57–72 (2020). https://doi.org/10.1007/s11010-020-03833-4

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