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Gestational Diabetes and Neutrophil Activation: A Cellular Symphony

Article in International Journal of Current Research in Medical Sciences · March 2024

DOI: 10.22192/ijcrms.2024.10.02.004

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 Int. J. Curr. Res. Med. Sci. (2024). 10(2): 26-38

International Journal of Current Research in

Medical Sciences
ISSN: 2454-5716
(A Peer Reviewed, Indexed and Open Access Journal)
www.ijcrims.com

Review Article Volume 10, Issue 2 -2024

DOI: http://dx.doi.org/10.22192/ijcrms.2024.10.02.004

Gestational Diabetes and Neutrophil Activation:

A Cellular Symphony
*
Emmanuel Ifeanyi Obeagu1 and Getrude Uzoma Obeagu2
1
Department of Medical Laboratory Science, Kampala International University, Uganda.
2
School of Nursing Science, Kampala International University, Uganda.
*
Corresponding authour: Emmanuel Ifeanyi Obeagu, Department of Medical Laboratory Science,
Kampala International University, Uganda,
[email protected], ORCID: 0000-0002-4538-0161

Abstract
Gestational diabetes mellitus (GDM) represents a complex metabolic disorder during pregnancy, impacting both
maternal and fetal health. Recent investigations have shed light on the intricate interplay between gestational diabetes
and neutrophil activation, revealing a cellular symphony that contributes to the pathophysiology of this condition.
This review explores the current state of knowledge regarding the relationship between gestational diabetes and
neutrophil activation, focusing on the molecular mechanisms, immune responses, and inflammatory cascades that
orchestrate this cellular symphony. Understanding these interactions is crucial for unraveling the complexities of
gestational diabetes and may pave the way for novel therapeutic interventions aimed at mitigating the associated
inflammatory burden and improving pregnancy outcomes.

Keywords: Gestational Diabetes, Neutrophil Activation, Immune Response, Inflammation, Pregnancy

Complications, Hyperglycemia, Cellular Dysfunction

Introduction GDM, affecting approximately 7% of pregnancies

globally, represents a multifaceted challenge in
Gestational diabetes mellitus (GDM) is a maternal-fetal medicine. The condition arises
significant health concern affecting a substantial from the inability of the maternal body to meet
number of pregnant women worldwide. the increased insulin demands during pregnancy,
Characterized by glucose intolerance first leading to elevated blood glucose levels. While
identified during pregnancy, GDM poses risks not GDM typically resolves after childbirth, it poses
only to maternal health but also to the developing immediate risks to both mother and child and is
fetus. Beyond its well-documented metabolic associated with a heightened risk of developing
implications, recent research has uncovered a type 2 diabetes later in life.1-20
compelling connection between gestational
diabetes and the activation of neutrophils, Neutrophils, as essential components of the
fundamental players in the innate immune system. immune system, play a crucial role in defending
26
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the host against infections. Pregnancy induces fetus. Hormones such as human placental
dynamic changes in the immune system to lactogen (hPL), progesterone, and cortisol
accommodate the growing fetus, and neutrophils contribute to insulin resistance, promoting
undergo alterations in phenotype and function glucose availability for fetal development.
during this period. However, disruptions in this However, in susceptible individuals, this insulin
delicate balance, as observed in gestational resistance can become exacerbated, leading to
diabetes, can lead to aberrant neutrophil impaired glucose tolerance.The pancreatic beta
activation, contributing to an inflammatory milieu cells, responsible for insulin secretion, face
with potential implications for pregnancy increased demands during pregnancy. In GDM,
outcomes.21-30 The rationale behind investigating these cells may struggle to produce sufficient
neutrophil activation in the context of gestational insulin to overcome the heightened insulin
diabetes is grounded in the growing recognition of resistance. This beta-cell dysfunction results in
the immune system's involvement in the inadequate insulin secretion, further contributing
pathophysiology of GDM. Neutrophils, to elevated blood glucose levels.31-45
traditionally viewed as frontline defenders against
microbial threats, have recently been implicated Inflammation and alterations in adipokine levels
in the inflammatory processes associated with contribute significantly to the pathophysiology of
metabolic disorders, including diabetes. GDM. Adipose tissue, particularly visceral
Understanding how hyperglycemia and other adipose tissue, secretes adipokines such as
factors related to gestational diabetes influence adiponectin and leptin. In GDM, an imbalance in
neutrophil behavior is pivotal for unraveling the adipokine production occurs, fostering a pro-
complexities of this cellular interplay. inflammatory environment. This inflammation,
characterized by increased levels of cytokines like
This review aims to provide a comprehensive tumor necrosis factor-alpha (TNF-α) and
exploration of the intricate connections between interleukin-6 (IL-6), is implicated in insulin
gestational diabetes and neutrophil activation, resistance and the progression of GDM.Persistent
unraveling the molecular mechanisms, immune hyperglycemia in GDM leads to the generation of
responses, and inflammatory cascades that reactive oxygen species (ROS) and oxidative
collectively form a cellular symphony. By delving stress. Elevated glucose levels induce
into the current state of knowledge, this review mitochondrial dysfunction and endoplasmic
seeks to contribute to a deeper understanding of reticulum stress, contributing to the production of
the pathophysiology of gestational diabetes, with ROS. Oxidative stress, in turn, exacerbates insulin
potential implications for novel therapeutic resistance and damages pancreatic beta cells,
interventions to mitigate the associated creating a feedback loop that perpetuates the
inflammatory burden and improve pregnancy hyperglycemic state.Inflammatory mediators,
outcomes. such as cytokines and chemokines, can interfere
with insulin signaling pathways, contributing to
Pathophysiology of Gestational Diabetes insulin resistance. These immune responses may
involve activation of nuclear factor-kappa B (NF-
Gestational diabetes mellitus (GDM) manifests as κB) and c-Jun N-terminal kinase (JNK) pathways,
a state of glucose intolerance during pregnancy, impairing insulin receptor signaling and
affecting both maternal and fetal health. The downstream glucose uptake.The pro-
pathophysiology of GDM is complex, involving inflammatory milieu associated with GDM,
intricate interactions between hormonal, characterized by elevated cytokines and oxidative
metabolic, and immunological factors.GDM often stress, has implications for immune cell function.
arises due to increased insulin resistance, a Neutrophils, key players in the innate immune
condition where cells exhibit reduced system, may undergo aberrant activation and
responsiveness to insulin. Pregnancy induces functional alterations in response to these
physiological changes aimed at ensuring an inflammatory signals, contributing to the intricate
adequate supply of nutrients for the growing cellular symphony associated with GDM.46-73
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Neutrophil Activation in Pregnancy contribute to placental development through

interactions with trophoblasts and vascular
The physiological adaptations during pregnancy remodeling. Their roles extend beyond immune
extend to the immune system, where dynamic defense to actively participating in tissue
changes in neutrophil function play a pivotal role. homeostasis and adaptation during
Neutrophils, as integral components of the innate pregnancy.While physiological neutrophil
immune system, undergo modifications in activation is a hallmark of healthy pregnancy, the
phenotype and behavior to accommodate the presence of gestational diabetes may disrupt this
unique requirements of pregnancy. Pregnancy delicate balance. Hyperglycemia and the
induces alterations in the circulating neutrophil associated inflammatory milieu in GDM could
population. Studies have shown an increase in potentially influence neutrophil function, leading
neutrophil counts during normal pregnancy, to aberrant activation, altered cytokine
reflecting the heightened demand for immune production, and impaired immune tolerance.
surveillance. These neutrophils may exhibit Investigating these potential deviations is crucial
changes in surface receptors, adhesion molecules, for deciphering the cellular symphony that
and migratory patterns to facilitate their roles in unfolds in the context of GDM.84-96
host defense and tissue remodeling.
Physiologically activated neutrophils in Molecular Mechanisms Linking
pregnancy demonstrate enhanced phagocytosis Hyperglycemia and Neutrophil Activation
and bactericidal activity. This heightened
functionality is thought to be a protective Hyperglycemia, a hallmark of gestational diabetes
mechanism, ensuring the maternal immune mellitus (GDM), is implicated in a multitude of
system is well-equipped to respond to potential molecular changes that extend beyond metabolic
infections that could compromise the health of pathways.97 In the context of neutrophil
both the mother and the developing fetus.73-83 activation, hyperglycemia can instigate a cascade
of events at the cellular and molecular levels,
Neutrophils in pregnancy display a degree of influencing the behavior and functionality of
immune tolerance, preventing unwarranted these immune effectors. Elevated glucose levels
immune responses against fetal antigens. This in GDM contribute to increased production of
tolerance is crucial for the protection of the semi- reactive oxygen species (ROS) within neutrophils.
allogeneic fetus from maternal immune attack. The excess glucose serves as a substrate for
Dysregulation in this balance can lead to adverse various enzymatic reactions, including the
pregnancy outcomes, including conditions like NADPH oxidase pathway. The heightened
preeclampsia. Hormones associated with activity of NADPH oxidase results in an
pregnancy, such as progesterone and estradiol, overproduction of ROS, leading to oxidative
exert immunomodulatory effects on neutrophils. stress. This oxidative milieu can activate redox-
These hormones influence the expression of sensitive signaling pathways and modulate
adhesion molecules, cytokine production, and the neutrophil functions. Hyperglycemia triggers the
overall responsiveness of neutrophils. Proper activation of specific isoforms of Protein Kinase
hormonal regulation is essential for maintaining C (PKC) within neutrophils. The activated PKC
an appropriate balance between immune tolerance isoforms participate in the phosphorylation of
and defense. Neutrophil extracellular traps various proteins involved in signal transduction,
(NETs) are web-like structures composed of altering cellular responses. This includes the
DNA, histones, and antimicrobial proteins that activation of the NADPH oxidase complex,
neutrophils release to trap and neutralize amplifying ROS production. Excessive glucose
pathogens. During pregnancy, NET formation can also divert into the polyol pathway, where it
may be heightened, serving as an additional is metabolized to sorbitol by the enzyme aldose
defense mechanism against infections. However, reductase. The accumulation of sorbitol can lead
dysregulated NET release has been implicated in to osmotic stress and the depletion of NADPH,
conditions such as preeclampsia. Neutrophils
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further contributing to oxidative stress within aberrant activation, leading to enhanced oxidative
neutrophils. stress and inflammatory responses.
Hyperglycemia-induced changes in neutrophil
Hyperglycemia promotes the formation of function can impact chemotaxis and phagocytosis.
Advanced Glycation End Products (AGEs) Neutrophils from individuals with GDM may
through non-enzymatic glycation reactions.98 exhibit impaired chemotactic responses, leading
AGEs can bind to their receptors (RAGE) on to compromised migration to sites of infection or
neutrophils, activating intracellular signaling inflammation. Additionally, alterations in
pathways and promoting inflammatory responses. phagocytic capabilities may contribute to an
This interaction can enhance the production of inadequate clearance of pathogens. The intricate
pro-inflammatory cytokines and perpetuate an balance between immune tolerance and defense
inflammatory environment. The NF-κB signaling mechanisms is crucial for a healthy pregnancy.
pathway, a central regulator of inflammation, is GDM disrupts this equilibrium, potentially
activated in response to hyperglycemia. Elevated leading to impaired immune tolerance against
glucose levels can induce the translocation of NF- fetal antigens and an increased risk of
κB to the nucleus, promoting the expression of inflammatory conditions such as preeclampsia.
genes involved in inflammation. Neutrophils, Neutrophils, as key contributors to immune
under the influence of hyperglycemia, may tolerance, may undergo dysregulated activation in
exhibit increased NF-κB activity, contributing to response to altered cytokine profiles.
enhanced production of inflammatory mediators.
Hyperglycemia-induced changes in cellular The NF-κB pathway, activated by hyperglycemia,
structure and function extend to the cytoskeleton contributes to the upregulation of pro-
of neutrophils. Actin polymerization, crucial for inflammatory mediators.100 This pathway is
processes such as chemotaxis and phagocytosis, central to the coordination of immune responses,
may be altered, impacting the migratory and and its dysregulation in GDM may result in a
phagocytic capabilities of neutrophils.Elevated sustained and heightened inflammatory state.
glucose levels can modulate the expression of Neutrophils, responding to this inflammatory
adhesion molecules on neutrophils, affecting their milieu, may exhibit increased activation and
ability to adhere to endothelial cells and migrate prolonged survival. Toll-like receptors (TLRs)
to sites of inflammation. This altered adhesion play a crucial role in recognizing pathogen-
and migration may contribute to the dysregulated associated molecular patterns (PAMPs) and
immune responses observed in GDM. initiating immune responses. In GDM, TLR
signaling may be dysregulated, influencing the
Immune Responses in GDM responsiveness of neutrophils to microbial
challenges. This altered TLR signaling can
The impact of gestational diabetes mellitus contribute to an imbalanced immune response in
(GDM) on immune responses extends beyond the the presence of infection.GDM is associated with
molecular alterations associated with alterations in the adaptive immune response,
hyperglycemia.99 The dysregulated immune including changes in T cell subsets and cytokine
milieu in GDM involves intricate interactions profiles. The crosstalk between adaptive and
between various immune cells, cytokines, and innate immunity is integral to mounting effective
signaling pathways. GDM is characterized by an immune responses. Dysregulation in adaptive
upregulation of pro-inflammatory cytokines, immunity in GDM may impact the priming and
including tumor necrosis factor-alpha (TNF-α), activation of neutrophils, influencing their roles in
interleukin-6 (IL-6), and interleukin-1β (IL-1β). immune defense and inflammation.The
These cytokines are not only implicated in the heightened oxidative stress and inflammatory
pathogenesis of insulin resistance but also environment in GDM may influence neutrophil
contribute to the systemic inflammatory milieu extracellular trap (NET) formation. While NETs
observed in GDM. Neutrophils, under the serve as an antimicrobial defense mechanism,
influence of these cytokines, may undergo dysregulated NET release has been implicated in
29
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vascular complications, linking the immune mechanisms crucial for maintaining pregnancy
responses in GDM to potential adverse pregnancy until term. The disruption of immune
outcomes. homeostasis, along with the potential activation of
neutrophils, could contribute to preterm birth.
Inflammatory Cascades and Pregnancy Altered neutrophil functions and dysregulated
Complications cytokine profiles may play a role in initiating
labor prematurely.
The intricate interplay between gestational
diabetes mellitus (GDM) and neutrophil Conclusion
activation sets the stage for inflammatory
cascades that can impact various aspects of Inflammatory mediators released in response to
pregnancy.101 The dysregulated immune GDM and neutrophil activation may impact fetal
responses and sustained inflammation associated growth by influencing nutrient transport and
with GDM may contribute to a range of placental function. This can lead to fetal growth
pregnancy complications, influencing both restriction, a condition associated with adverse
maternal and fetal well-being.GDM is perinatal outcomes. The dysregulated immune
characterized by an inflammatory milieu marked responses in GDM, including the potential
by the dysregulated secretion of pro-inflammatory aberrant activation of neutrophils, contribute to a
cytokines and chemokines. Neutrophils, activated spectrum of adverse pregnancy outcomes. These
in response to hyperglycemia, contribute to this may encompass not only preeclampsia, preterm
cytokine storm by releasing inflammatory birth, and fetal growth restriction but also an
mediators. Elevated levels of cytokines such as increased risk of gestational hypertension and
tumor necrosis factor-alpha (TNF-α) and cesarean section. The symphony of gestational
interleukin-6 (IL-6) create an inflammatory diabetes mellitus (GDM) and neutrophil
environment that extends beyond the local site of activation orchestrates a complex interplay that
neutrophil activation. The sustained inflammatory influences the course of pregnancy. This review
state associated with GDM can negatively impact has delved into the molecular mechanisms linking
placental function. Chronic inflammation may hyperglycemia to neutrophil activation, explored
disrupt the delicate balance required for normal the immune responses in GDM, and deciphered
placental development, potentially leading to the inflammatory cascades that contribute to
complications such as impaired nutrient various pregnancy complications.
exchange, oxidative stress, and alterations in the
expression of growth factors crucial for fetal GDM, marked by elevated glucose levels,
development. Inflammatory cascades initiated by instigates a series of molecular events within
GDM and exacerbated by neutrophil activation neutrophils. Hyperglycemia-induced reactive
can contribute to endothelial dysfunction, a key oxygen species (ROS) production, activation of
feature of conditions like preeclampsia. The protein kinase C (PKC) isoforms, and the
release of inflammatory mediators, coupled with formation of advanced glycation end products
oxidative stress, may compromise vascular (AGEs) contribute to a pro-inflammatory milieu.
integrity, leading to hypertension, proteinuria, and These molecular alterations, in turn, modulate
impaired blood flow, characteristic of neutrophil functions, impacting their roles in
preeclampsia. Inflammatory signals generated in immune surveillance and host defense. The
response to GDM and neutrophil activation can immune responses in GDM are characterized by
contribute to insulin resistance, not only in the dysregulated cytokine and chemokine release,
mother but also in the developing fetus. This fetal creating an inflammatory environment that
exposure to an inflammatory environment may extends beyond the local activation of neutrophils.
contribute to long-term metabolic programming, This chronic inflammation is implicated in
increasing the risk of obesity and diabetes in the various pregnancy complications, including
offspring later in life. Chronic inflammation in placental dysfunction, endothelial dysfunction
GDM may compromise immune tolerance leading to preeclampsia, insulin resistance,
30
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Emmanuel Ifeanyi Obeagu and Getrude Uzoma Obeagu. (2024). Gestational Diabetes and Neutrophil
Activation: A Cellular Symphony. Int. J. Curr. Res. Med. Sci. 10(2): 26-38.
DOI: http://dx.doi.org/10.22192/ijcrms.2024.10.02.004

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