Expression of surfactant proteins SP-A and SP-D in murine decidua and immunomodulatory effects on decidual macrophages

Madhukaran, Shanmuga Priyaa; Gopalakrishnan, Arun; Pandit, Hrishikesh; Marri, Eswari; Kouser, Lubna; Jamil, Kaiser; Alhamlan, Fatimah S.; Kishore, Uday; Madan, Taruna

doi:10.1016/j.imbio.2015.09.019

Cited by 13 publications

(10 citation statements)

References 59 publications

(64 reference statements)

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“…Conversely, injecting anti-SP-A antibodies into the mice amniotic sac can delay parturition by up to 24 hours (Condon et al, 2004). The view by Condon et al that fetal SP-A triggers the onset of labor is consistent with our recent finding that SP-A and SP-D levels are low during pre-(17.5dpc) and near (19.5 dpc) parturition in the murine decidua (Madhukaran et al, 2015c). Despite the elevated SP-A and SP-D levels in the AF at term, the transcript level of decidual (maternal) SP-A was absent.…”

Section: Sp-a and Sp-dsupporting

confidence: 90%

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Role of collectins and complement protein C1q in pregnancy and parturition

et al. 2016

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Collectins such as surfactant proteins SP-A, SP-D, and mannan-binding lectin (MBL), as well as complement protein C1q are evolutionarily conserved innate immune molecules. They are known to opsonize a range of microbial pathogens (bacteria, fungi, virus, and parasites) and trigger effector clearance mechanisms involving phagocytosis and/or complement activation. Collectins and C1q have also attracted attention in studies involving pregnancy as they are expressed in the female reproductive tissues during pregnancy; a unique state of immune suppression with increased susceptibility to infectious diseases. Recent studies are beginning to unravel their functional significance in implantation, placentation, pregnancy maintenance and parturition in normal and adverse pregnancies. Collectins and C1q, expressed in gestational tissues during pregnancy, might alter the status of mother's immune response to the allogenic fetus and the microenvironment, thereby serving as important regulators of fetus-mother interaction. Here, we discuss the functional roles that have been assigned to SP-A, SP-D, MBL and C1q in pregnancy and parturition.

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Section: Sp-a and Sp-dsupporting

confidence: 90%

“…In contrast, SP-D levels were found to decrease with the gestation age from 17.5 dpc to 19.5 dpc in murine decidua (Madhukaran et al, 2015c). We suspect that increased SP-D level at 17.5 dpc could reflect paracrine effect on fetal membrane, cervix and myometrium involved in hindering prostaglandin E2 activation required for labor.…”

Section: Sp-a and Sp-dmentioning

confidence: 80%

Role of collectins and complement protein C1q in pregnancy and parturition

et al. 2016

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“…However, SP-A plays a dual role in this scenario as it enhances dendritic cell-mediated transfer of HIV in vitro [32]. Studies on the role of SPs during pregnancy suggested that SP-A and SP-D had a protective function in the murine decidua; and it was proposed that exogenous administration of SP-A (and SP-D) could potentially control infection during spontaneous term labor and infection-induced preterm labor [45].…”

Section: Discussionmentioning

confidence: 99%

Surfactant Protein A Impairs Genital HPV16 Pseudovirus Infection by Innate Immune Cell Activation in A Murine Model

et al. 2019

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Infection by oncogenic human papillomavirus (HPV) is the principle cause of cervical cancer and other anogenital cancers. The majority of cervical cancer cases occur in low- and middle-income countries (LMIC). Prophylactic vaccines exist to combat HPV infection but accessibility to these in LMIC is limited. Alternative preventative measures against HPV infection are therefore also needed to control cervical cancer risk. HPV employs multiple mechanisms to evade the host immune response. Therefore, an approach to promote HPV recognition by the immune system can reduce infection. Surfactant proteins A and D (SP-A and SP-D) are highly effective innate opsonins of pathogens. Their function is primarily understood in the lung, but they are also expressed at other sites of the body, including the female reproductive tract (FRT). We hypothesized that raised levels of SP-A and/or SP-D may enhance immune recognition of HPV and reduce infection. Co-immunoprecipitation and flow cytometry experiments showed that purified human SP-A protein directly bound HPV16 pseudovirions (HPV16-PsVs), and the resulting HPV16-PsVs/SP-A complex enhanced uptake of HPV16-PsVs by RAW264.7 murine macrophages. In contrast, a recombinant fragment of human SP-D bound HPV16-PsVs weakly and had no effect on viral uptake. To assess if SP-A modulates HPV16-PsVs infection in vivo, a murine cervicovaginal challenge model was applied. Surprisingly, neither naïve nor C57BL/6 mice challenged with HPV16-PsVs expressed SP-A in the FRT. However, pre-incubation of HPV16-PsVs with purified human SP-A at a 1:10 (w/w) ratio significantly reduced the level of HPV16-PsV infection. When isolated cells from FRTs of naïve C57BL/6 mice were incubated with HPV16-PsVs and stained for selected innate immune cell populations by flow cytometry, significant increases in HPV16-PsVs uptake by eosinophils, neutrophils, monocytes, and macrophages were observed over time using SP-A-pre-adsorbed virions compared to control particles. This study is the first to describe a biochemical and functional association of HPV16 virions with the innate immune molecule SP-A. We show that SP-A impairs HPV16-PsVs infection and propose that SP-A is a potential candidate for use in topical microbicides which provide protection against new HPV infections.

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“…This is especially important in ensuring successful pregnancies, as these infections can lead to complications of pregnancy such as premature birth, still birth and neonatal sepsis [29] . In pregnancy, SP-A and SP-D are present in the amniotic fluid, placenta, amnion and chorion [23,30] .…”

Section: The Female Reproductive Tractmentioning

confidence: 99%

“…Expression of SP-A and SP-D is elevated in the first trimester decidua (maternal part of the placenta) by trophoblasts and decidual stromal cells [31] . The potential function of this increase in SP-A and SP-D in protection from bacterial infection is supported by the SP-A-and SP-D-mediated reduction of lipopolysaccharide (LPS)-induced inflammation associated with TNF-α release by decidual macrophages [29] . At term, SP-A has been shown to decrease in the amniotic fluid, possibly due to it being sequestered by receptors in the amnion [32] .…”

Section: The Female Reproductive Tractmentioning

confidence: 99%

Non-Pulmonary Immune Functions of Surfactant Proteins A and D

Ujma

Horsnell²,

Katz³

et al. 2016

J Innate Immun

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Surfactant proteins A (SP-A) and D (SP-D) are established as essential components of our innate immune system for protecting the lung from pathogens and allergens. They essentially exert their protective functions by regulating pulmonary homeostasis. Both proteins are however widely expressed throughout the body, including the female reproductive tract, urinary tract, gastrointestinal tract, the eye, ear, nasal compartment, central nervous system, the coronary artery and the skin. The functions of SP-A and SP-D at these sites are a relatively underinvestigated area, but it is emerging that both SP-A and SP-D contribute significantly to the regulation of inflammation and protection from infection at these sites. This review presents our current understanding of the roles of SP-A and SP-D in non-pulmonary sites.

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Expression of surfactant proteins SP-A and SP-D in murine decidua and immunomodulatory effects on decidual macrophages

Cited by 13 publications

References 59 publications

Role of collectins and complement protein C1q in pregnancy and parturition

Role of collectins and complement protein C1q in pregnancy and parturition

Surfactant Protein A Impairs Genital HPV16 Pseudovirus Infection by Innate Immune Cell Activation in A Murine Model

Non-Pulmonary Immune Functions of Surfactant Proteins A and D

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