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The Journal of Theoretical Fimpology. Volume 1, Issue 2: e-20120609-1-2-3. May 18, 2013 (www.fimpology.com)

Six Models of Pregnancy-Associated Eukaryotic Cell Transmission among Fetus, Mother and Infant

Shu-dong Yin

ORCID ID: https://orcid.org/0009-0005-8661-6889

Cory H. E. R. & C. Inc., Burnaby, British Columbia, Canada
Email: [email protected]

Abstract

Pregnancy-associated cell transmission among fetus, mother and infant has attracted more and more attention during the past decades, among which, fetus-to-maternal cell transmission (FMCT) and maternal-to-fetal cell transmission (MFCT) are the two most studied. Recently, a novel model called fetus-breastmilk-breastfeeding-infant-cells cycle (FBBIC Cycle) has been proposed, which uncovered an unrecognized embryonic/fetal cell migration for the transmission of eukaryotic cells from fetus to infant him/herself via breastmilk and breastfeeding. Up to now, total six models: (i) FMCT, (ii) MFCT, (iii) gestation-associated fetus-to-fetus cell transmission (FFCT), (iv) breastmilk and breastfeeding-mediated maternal-to-infant cell transmission (MICT), (v) breastmilk and breastfeeding-mediated fetus-to-infant allogenic or inter-sibling cell transmission (FICT), and (vi) FBBIC Cycle constitute a complex system of eukaryotic cell exchange and interaction among mother, fetus and suckling infant during gestation and lactation. Among these pregnancy-associated models, FBBIC Cycle should be the major melody because only it reflects the most benefit of offspring during his/her prenatal and postnatal life in the physiological and immunological perspective without potential disadvantages introduced by allogenic and semi-allogenic cells. A thoroughly theoretical exploration in fimpology is essential to accurately interpreting prenatal diagnosis, making further development of molecular diagnostic techniques and deeply elucidating tolerogenic mechanisms in transplantation immunology.

Key Words: cell transmission; pregnancy; breastfeeding; FBBIC Cycle; microchimerism; maternal cells; fetal cells; stem cells; milkcells

Introduction

Based on the existing data from studies on humans and non-human mammals, six models of eukaryotic cell transmission among mother, fetus and infant during gestation and lactation have been proposed although some need further direct supporting evidences: (i) gestation-associated embryonic/fetal cell migration into maternal body (FMCT), which results in fetal-maternal microchimerism (FMMC) (64,79,80,139-141); (ii) gestation-associated maternal cell migration into fetal body (MFCT), which results in maternal-to-fetal microchimerism (MFMC) (28,34,36,85,142,143); (iii) gestation-associated allogenic or inter-sibling fetal cell transmission between different fetuses (FFCT), or called "transmaternal sibling microchimerism" which results in fetofetal microchimerism (FFMC) (94-100,104); (iv) gestation and lactation-associated maternal host cell migration into the body of suckling infant via breastmilk and breastfeeding (MICT), which results in maternal-infantile microchimerism (MIMC) (30,84,89,106,110,111,144,145); (v) gestation and lactation-associated allogenic or inter-sibling fetal cell transmission to the suckling infant via breastmilk and breastfeeding (FICT), which results in fetoinfantile microchimerism (FIMC); and (vi) gestation and lactation associated fetus-to-infant his/her own fetal cell external transmission via breastmilk and breastfeeding, or called Fetus-Breastmilk-Breastfeeding-Infant-Cells Cycle (FBBIC Cycle) (82) (see Figure).
Interestingly, FMCT, MFCT, FFCT, MICT and FICT share a common characteristic that is the migration of foreign cells into tissues and/or organs of a macroorganism body. MFCT, FMCT, and FFCT occur during gestation, and MICT and FICT may take place postnatally in those infants who were breastfed with their own mothers' breastmilk, or with breastmilk from allogenic lactating mothers or donors.
In mammals including human beings, there are three major naturally connected physiological proceedings for producing offspring — (i) embryonic/fetal growth and development, (ii) production of breastmilk, and (iii) breastfeeding offspring. However, MFCT, FMCT, FFCT, MICT and FICT fail to reflect the physiological importance and the biological necessity for the continuity of these natural events. Only can FBBIC Cycle satisfy the most benefit of offspring during their prenatal and postnatal life in the physiological and immunological perspective, and therefore, should be recognized as the major physiological mechanism in these models. In this manuscript, these different models of pregnancy-associated prenatal and postnatal cell transmission are briefly summarized.

I. Migration of Embryonic/Fetal Cells into Maternal Body (FMCT)

Migration of fetal cells into maternal organs and tissues (FMCT), or called fetomaternal microchimerism (FMMC) was the earliest recognized consequence of cellular migration from fetus to mother, and was first described by Georg Schmorl in a pathological case in 1893 (58,59). Studies on humans and non-human mammals indicated that migration of fetal cells into maternal blood is a normal physiological phenomenon that occurs in all pregnancies (15,59-61).

Detection of fetal cells in maternal body

The earliest presence of fetal cell in maternal body varied in different species. In murine model, fetal microchimerism begins soon after implantation, and increases with gestational age (9,15,16,18,23,60,62). In humans, the earliest detectable fetal cells in the body of normal pregnant women reported by different research groups was at 4-5 week- (3), 6 week- (63), and 15 week-gestational age (64) respectively.
Migration of fetal cell into maternal organs/tissues in humans appeared to increase with gestational age (24). The number of fetal cells in maternal blood varied widely ranging from one fetal cell per 10[4] to one fetal cell per 10[9] maternal cells (6). Lo and colleagues even showed that at least 17% of maternal cellular component was positive for fetal DNA (65).
Many maternal tissues and organs of humans and some non-human mammal models were showed to harbor fetal cells (see Table 1); and moreover, those co-existing fetal cells were found to be multiple cell types including endothelial cells, mesenchymal stem cells /progenitors and neuronal cells in the relevant maternal tissues and organs (see Table 2).

Clinical significance and potential challenge

The potential physiological significance and pathological consequence of FMCT has been one of reasons for attracting researchers' attention during the past two decades (55,59,63,66-68). The existing literatures indicted that fetal cells seemed to involve in the pathogenesis of some clinical diseases, such as preeclampsia, rheumatoid arthritis, systemic lupus erythematosus (SLE) and systemic sclerosis during pregnancy (7,13,66,67,69-74), or possibly to play a role in maternal tissue repair during and after gestation (13,22,26,63,75,76). O'Donoghue even proposed that the co-existence of fetal cells in maternal body may be one of answers for the question of "Why is maternal life longer than paternal life?" (78).
The possible role played by fetal cells in anti-breast cancer attracted Gadi and colleagues' attention (79-81). However, while elucidating the anti-breast-cancer hypothesis, Gadi revealed that fetal cells co-existed in normal breast tissue of parous healthy women (17), which, to the best of my knowledge, may be the first direct supporting evidence of the FBBIC Cycle theory (82).
Another reason for study on FMCT is its potential value in prenatal genetic diagnosis (4,8,78). However, upon possible FFCT and FMCT from silent aborted pregnancies or elder siblings, how to interpret properly the results of prenatal genetic diagnosis is a challenge although Sato and colleagues showed that after abortion, a quick decline of fetal cells in the maternal blood circulation to an undetectable level needed only one month (83).

II. Migration of Maternal Cells into Fetal Body (MFCT)

Gestational maternal immunity transmission to fetus was described as early as in 1892 by Paul Erlich using experimental mouse models (59,84). Although the distinction between humoral and cellular immunities hadn't established until the emergence of modern immunology during the second half of the 20th century, some researchers believed that in Paul Erlich's mouse models, the transmission of maternal cell-mediated cellular immunity to fetus should be included (59,84). Maloney and colleagues further showed that maternal cells even persisted in the body of healthy offspring for as long as 49 years (59,85), which, therefore, has been recognized as a physiological phenomenon (59). Studies on humans and some non-human mammals showed that maternal cells were found in multiple tissues and organs of fetal, neonatal and adult offspring (see Table 1). Many maternal cell lineages that were found in offspring tissues and organs include erythrocytes, leukocytes (granulocytes, T and B lymphocytes) and platelets (see Table 2).

Clinical significance

The first impression of maternal cells in the body of offspring was associated with their pathological role (59,86,87). Microchimeric maternal cells in offspring may involve in the pathogenesis of some pediatric diseases, such as neonatal lupus syndrome (34,68,73), juvenile dermatomyositis (68,88), and type 1 diabetes (41). Moreover, the migration of maternal cells into fetal body was considered to be a prenatal mechanism for the vertical transfer of viral pathogens (89,90).

Maternal-donor related renal transplant

As early as in 1950s, animal experiments and clinical studies showed that maternal eukaryotic cells within fetal body may involve in tolerance genesis (91). The tolerance to noninherited maternal antigens (NIMAs) through the exposure to maternal cells in fetal body was proposed as one of tolerogenic mechanisms (89,92,93). However, in mammals including human beings, the exposure to NIMAs may occur during gestation and/or lactation via the following routes: (i) molecular exchange between mother and fetus, and/or between lactating mother and her suckling infant, and (ii) migration of maternal cells into fetal body, and/or migration of maternal cells into the body of her suckling infant, which depends on whether the infant being breastfed by his/her own mother. Therefore, at the cellular level, the tolerance to NIMAs may occur as early as during gestation via MFCT. Postnatal MICT may play a role in strengthening the tolerance to NIMAs. More discussion is in the following MICT section.

III. Gestation-Associated Fetal Cell Transmission between Different Fetuses (FFCT)

In the gestational fetus-to-fetus fetal cell transmission (FFCT) model, "Fetuses" are different individuals, and fetal cells from one fetus can co-exist within fetal body/bodies of the other/others. FFCT could occur theoretically in the following pregnant circumstances: (i) multiple pregnancies including twin pregnancy (94-98), in which, more than one fetus are usually growing and developing simultaneously within one uterus; (ii) residual fetal cells in maternal body from previously aborted embryo enter the body of another fetus of next pregnancy (99,100); and (iii) remaining fetal cells in maternal body from previously born brothers and/or sisters migrate into fetal body of younger brothers and/or sisters (101,102).
It is worth to point out that FFCT in the existing literatures of animal study on microchimerism has been often overlooked. In fact, many non-human mammal models used in experimental studies are multiple pregnancy animals, such as mice, rats, and pigs (103,104); and therefore, theoretically, there should be a fetus-to-fetus cell transmission or exchange during their normal gestation, which was supported by the latest laboratory evidences from studies on porcine littermates (103,104).
In humans, despite normal fetus-to-fetus microchimerism in plural pregnancy (94,98), there may be a FFCT in the extant pregnancy of multiparous women who previously experienced a silent or identified pregnancy. Nelson's group revealed an interesting phenomenon that male DNA or cells were often detected in healthy women who had never given birth to a son (99,100), for which, FFCT was discussed to be one of possible explanations by the authors (99).

Clinical significance

The inherited paternal antigens (IPAs) of one fetus in previous/or extant pregnancy may be noninherited paternal antigens (NIPA) to the other fetus of next/or extant pregnancy. The clinical significance of FFCT is elucidated in a noninherited-paternal-antigens-centric model for understanding transplantation immunology (see the article entitled "A Noninherited-Paternal-Antigens-Centric Model for the Birth Order and Sibship Size Effect in Transplantation Immunology" in this issue).
Offspring may contact NIPA via prenatal FFCT and postnatal FICT. Roelen and colleagues showed that no differences in the frequencies of cytotoxic T cell precursors (CTLp) and IL-2-producing helper T cell precursors (HTLp) against the noninherited maternal and the paternal HLA-A and -B antigens, and moreover, similar frequencies of CTLp and HTLp were observed between breastfed and non-breastfed children (105), which suggested the efficiency of gestational exposure to NIPA via prenatal FFCT may be superior to that of lactational exposure to NIPA via breastmilk and breastfeeding-mediated FICT. Perhaps, the significance of exposure to NIPA via postnatal FICT is in strengthening NIPA-tolerogenesis.

IV. Migration of Maternal Cells into Infantile Body (MICT)

Migration of maternal host cells into suckling body via breastmilk and breastfeeding, which results in maternal-infantile microchimerism (MIMC), was supported by many laboratory evidences from experimental studies on non-human mammals, such as murine (30,84,106-109), lambs (107), and piglets (110,111).
Traditionally, it was accepted generally during the 20th century that milkcells consisted of multiple end-differentiated maternal cell lineages, such as mononuclear phagocytes, polymorphonuclear leukocytes, lymphocytes, colostral corpuscles, and ductal/luminal epithelial cells. Such notion was reflected in almost all of the studies around milk cells (30,107,109,112-116). Recently, various stem/progenitor cells in breastmilk of human beings and non-human mammals were also assumed to be from maternal mammary stem cells (117-119), which was supported by that similar stem/progenitor cell properties were described on human breast epithelial cell line (120-123). Therefore, as the consequence, on the one hand, none of previous studies on breastfeeding-mediated cell transmission to offspring had further checked milkcells' origins; on the other hand, relevant laboratory techniques for distinguishing milkcells from different individuals haven't been developed yet. However, in the recently proposed FBBIC Cycle theory, milkcells were hypothesized to be heterogeneous and derived from both maternal and fetal sources (82). According to the new understanding, the co-existence of partial milkcells within the body of a suckling infant may be the consequence of MICT, FICT and FBBIC Cycle.

Clinical significance

In 1980s, some researchers found that breastfed patients who were the recipients of maternal-donor related renal transplant had better graft function rates than did non-breastfed counterparts (124,125), in which, the tolerance to noninherited maternal antigens (NIMAs) through the exposure to maternal cells via prenatal MFCT and postnatal MICT via breastfeeding was believed to be one of tolerogenic mechanisms (89,92,126).
However, comparing to MFCT, the real significance of MICT in the tolerance genesis to NIMAs needs further evaluation. Breastfeeding-mediated postnatal MICT may play a role as strengthening the tolerance to NIMAs as the strengthening immunization to a vaccine.

V. Migration of Sibling and Allogeneic Fetal Cells into Infantile Body (FICT)

Inter-sibling or allogeneic fetal cells transmission is defined to be a small amount of foreign fetal cells migrated into tissues or circulation of infants during lactation via breastfeeding, in which, "fetus" that fetal cells derived from and "infant" who harbored the fetal cells are not the same individual; and moreover, the fetal cells are not from the maternal host source.
It is not difficult to understand that the following three conditions were most likely to allow FICT to occur in a suckling infant: (i) the infant was breastfed by an allogeneic lactating mother; (ii) the infant was fed with donor breastmilk from Human Milk Bank; and (iii) the infant was breastfed by his/her own multiparous mother. In the above first two conditions, the obtained fetal cells by breastfed infant are allogeneic. In the third condition, the fetal cells left in breastmilk were derived from his or her siblings in previous pregnancies/abortions.
Theoretically, FICT and FBBIC Cycle may even occur simultaneously in infants who were breastfed by their own multiparous mothers. In other words, when breastfed by his/her own multiparous mother, suckling baby may regain two kinds of fetal cells: one is his or her own fetal cells defined under the FBBIC Cycle, and the other fetal cells left by his or her siblings in previous pregnancies/abortions. Even the possibility that FICT of some embryonic/fetal stem cells derived from maternal siblings and grandmother cannot be ruled out.
Embryonic stem cells were referred to those cells that come from an organism at its earliest stages of development (127), and can infinitely renew themselves and transform into multicellular lineages in the body of macroorganisms, such as human beings and non-human mammals (22,127).
Therefore, embryonic/fetal cells including stem cells in breastmilk theoretically may come from the following possible origins: (i) embryo/fetus of the extant pregnancy, (ii) embryonic/fetal siblings in extant multiple pregnancy, (iii) embryo/fetus of previously aborted or successful pregnancies, (iv) embryo/fetus of maternal siblings, (v) mother herself, and (vi) grandmother.

Clinical significance

To the best of my knowledge, it is the first time to theoretically propose that there may a FICT mechanism that may mediate sibling embryonic/fetal cells and allogeneic embryonic/fetal cells in breastmilk into the body of suckling infants via breastfeeding.
FICT may involve in tolerogenic mechanisms of transplantation immunology, which has been discussed in the article entitled "A noninherited-paternal-antigens-centric model for the birth order and sibship size effect in transplantation immunology" in this issue.

VI. Fetus-to-Infant His/Her Own Cells Transmission Cycle or Fetus-Breastmilk-Breastfeeding-Infant-Cells Cycle (FBBIC Cycle)

Recently, a model called Fetus-Breastmilk-Breastfeeding-Infant-Cells Cycle (FBBIC Cycle) was proposed for revealing an unrecognized mechanism (82), in which, "fetus" and "infant" in this model are the same individual, and moreover, the absorbed fetal cells from breastmilk were actually derived from the suckling infant's own host cells. Therefore, FBBIC Cycle reflects the fetus-to- infant his/her own cell external transmission via breastmilk and breastfeeding.
If an infant has never been breastfed by his/her own mother's breastmilk, his/her FBBIC Cycle may be missed (82). In fact, among the six different eukaryotic cell transmissions, only is FBBIC Cycle able to account for why the following three physiological events should be naturally connected: (i) embryonic/fetal growth and development, (ii) production of breastmilk and (iii) breastfeeding offspring.

Pregnancy-associated maternal immune protection blank (MIPB)

In humans, the gestational course from a fertilized egg to a matured fetus normally needs 37-40 weeks. In clinical medicine, pregnancies of less than 37 weeks or longer than 42 weeks are usually defined as a pathological status. During gestation, maternal body continuously contacts novel external foreign antigens including those in foods and air. It is well known that the establishment of immune to a specific antigenic stimulation usually needs 4 weeks.
During gestation, newly formed maternal immunity cannot be transferred to her offspring of extant pregnancy via DNA inheritance. However, such newly acquired maternal immune protection can be transferred to her offspring mainly via trans-placental IgG and possibly gestational MFCT. Therefore, the gestational period is a relative maternal immune protection blank (MIPB) for novel external foreign antigens for offspring, in which, there is a 4-week absolute MIPB for gestational offspring.
How does offspring overcome this MIPB period? FBBIC Cycle may be one of mechanisms for answering this question. During gestation, fetal cells migrate into the maternal blood circulation and other tissues/organs where they have an opportunity to contact the novel foreign antigens that the pregnant maternal body is experiencing. Normal pregnancy has been revealed to be a systemic Th2 characterized immune response in maternal body since 1993 (128). Moreover, studies on human breastmilk have already showed that there is certain amount of microorganisms in normal breastmilk including bacterial (129-132), fungal (146), and viral species (133-138), and therefore, any episodes of exposure to novel bacterial, viral and fungal agents or other foreign antigens during gestation may affect both maternal immune cells and those microchimeric fetal cells. Because some fetal cells are embryonic stem cells, and have the capability to differentiate into various cell lineages including immune cells (such as T memory cells, for example). If these fetal cells return the body of suckling infant via breastfeeding, doubtlessly, the acquired cellular immunity during gestation in maternal body will be transferred to postnatal suckling neonates.
It already has been proposed that fetal cell-derived maternal alloantigens-tolerogenic fetal T regulatory cells (MATF-TRCs) (35,37) and paternal alloantigens-tolerogenic fetal T regulatory cells (PATF-TRCs) (82) may involve in suppressing postnatal antimaternal or antipaternal immune reaction to maternal or paternal graft (82).

Conclusion

Eukaryotic cell transmission among fetus, mother and infant during pregnancy is a complex process, which covers both gestation and lactation. Up to now, total six pregnancy-associated cell transmission models have been proposed, among which, FBBIC Cycle is the only model that can satisfy the most benefit of offspring's prenatal and postnatal life in physiology and immunology, and account for the necessity and the continuity of gestation to lactation in pregnancy (82). Prenatal FFCT and postnatal FICT may involve in paternal alloantigens-tolerogenic mechanism of offspring. A thoroughly theoretical exploration in the quadruple relationship of fetus, infant, mother and father is one of the current major concerns of fimpology, which doubtlessly will contribute to interpretation of prenatal genetic diagnosis, development of molecular diagnostic techniques and elucidation of tolerogenic mechanisms in transplantation immunology.

Abbreviations

FMCT: gestation-associated fetus-to-maternal cell transmission;
MFCT: gestation-associated maternal-to-fetal cell transmission;
FFCT: gestation-associated fetus-to-fetus cell transmission;
MICT: breastmilk and breastfeeding-mediated maternal-to-infant cell transmission;
FICT: breastmilk and breastfeeding-mediated transmission of sibling and allogenic fetal cells into infantile body;
FBBIC Cycle: fetus-to-infant his/her own fetal cell external transmission via breastfeeding;
FMMC: fetal-maternal microchimerism;
MFMC: maternal-to-fetal microchimerism;
FFMC: fetofetal microchimerism;
MIMC: maternal-infantile microchimerism;
FIMC: fetoinfantile microchimerism;
NIPAs: noninherited paternal antigens;
NIMAs: noninherited maternal antigens.

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