Pulmonary macrophages and their different roles in health and disease

Melo, Eliza Mathias; Oliveira, Vívian Louise Soares de; Boff, Daiane; Galvão, Izabela

doi:10.1016/j.biocel.2021.106095

Cited by 16 publications

(11 citation statements)

References 124 publications

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“…To combat foreign pathogens, many immune defenders, primarily macrophages, are located in the lungs (Figure 1) (4, 10-12). Pulmonary macrophages phagocytize surfactants, inhaled stimuli/invaders, and apoptotic and fragmented cells to maintain lung homeostasis (133,134). Different microenvironments shape resident macrophages as distinct populations, such as alveolar macrophages (AMs, CD64 + MerTK + F4/80 + SiglecF hi/-CD169 +/-) and interstitial macrophages (IMs, LYVE1 lo/hi CD64 + MerTK + F4/80 + SiglecF -) (135).…”

Section: The Macrophage-alveolar Epithelial Cell Axis Regulates Pulmo...mentioning

confidence: 99%

The crosstalk between parenchymal cells and macrophages: A keeper of tissue homeostasis

Chen

2022

Front. Immunol.

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Non-parenchymal cells (NPCs) and parenchymal cells (PCs) collectively perform tissue-specific functions. PCs play significant roles and continuously adjust the intrinsic functions and metabolism of organs. Tissue-resident macrophages (TRMs) are crucial members of native NPCs in tissues and are essential for immune defense, tissue repair and development, and homeostasis maintenance. As a plastic-phenotypic and prevalent cluster of NPCs, TRMs dynamically assist PCs in functioning by producing cytokines, inflammatory and anti-inflammatory signals, growth factors, and proteolytic enzymes. Furthermore, the PCs of tissues modulate the functional activity and polarization of TRMs. Dysregulation of the PC‐TRM crosstalk axis profoundly impacts many essential physiological functions, including synaptogenesis, gastrointestinal motility and secretion, cardiac pulsation, gas exchange, blood filtration, and metabolic homeostasis. This review focuses on the PC‐TRM crosstalk in mammalian vital tissues, along with their interactions with tissue homeostasis maintenance and disorders. Thus, this review highlights the fundamental biological significance of the regulatory network of PC‐TRM in tissue homeostasis.

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Section: The Macrophage-alveolar Epithelial Cell Axis Regulates Pulmo...mentioning

confidence: 99%

The crosstalk between parenchymal cells and macrophages: A keeper of tissue homeostasis

Chen

2022

Front. Immunol.

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“…IL-33 also enhances the polarization of alternatively activated macrophages (AAM) [171,197], important in the resolution of inflammation and promotion of tissue repair post-IAV infection. Indeed, these macrophages are able to remove cellular debris and apoptotic cells after tissue injury and to avoid the further propagation of the inflammation by expressing suppressor receptors (such as PD-L1) and anti-inflammatory mediators (such as IL-10) [198,199].…”

Section: Il-33 Regulates Immune Responses During Iav Infectionmentioning

confidence: 99%

Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species

Rozario

Martínez-Sobrido

McSorley

et al. 2021

Viruses

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Influenza A viruses (IAVs) are important respiratory pathogens of horses and humans. Infected individuals develop typical respiratory disorders associated with the death of airway epithelial cells (AECs) in infected areas. Virulence and risk of secondary bacterial infections vary among IAV strains. The IAV non-structural proteins, NS1, PB1-F2, and PA-X are important virulence factors controlling AEC death and host immune responses to viral and bacterial infection. Polymorphism in these proteins impacts their function. Evidence from human and mouse studies indicates that upon IAV infection, the manner of AEC death impacts disease severity. Indeed, while apoptosis is considered anti-inflammatory, necrosis is thought to cause pulmonary damage with the release of damage-associated molecular patterns (DAMPs), such as interleukin-33 (IL-33). IL-33 is a potent inflammatory mediator released by necrotic cells, playing a crucial role in anti-viral and anti-bacterial immunity. Here, we discuss studies in human and murine models which investigate how viral determinants and host immune responses control AEC death and subsequent lung IL-33 release, impacting IAV disease severity. Confirming such data in horses and improving our understanding of early immunologic responses initiated by AEC death during IAV infection will better inform the development of novel therapeutic or vaccine strategies designed to protect life-long lung health in horses and humans, following a One Health approach.

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“…Being the most abundant innate immune cell in the alveolar spaces of the lungs [ 12 ], AM are the first line of defense against infections and invaders, recognizing pathogen-associated molecular patterns, such as LPS from Gram-negative bacteria. They are able to phagocytose and eliminate these pathogens and release pro-inflammatory cytokines to induce immune cell recruitment and the development of the inflammation [ 13 ]. Additionally, AM are very important in the late stages of ARDS since the depletion of these cells has been linked with decreased efferocytosis and lowered control of inflammation [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Absence of CCR2 Promotes Proliferation of Alveolar Macrophages That Control Lung Inflammation in Acute Respiratory Distress Syndrome in Mice

Oliveira

Pollenus

Berghmans

et al. 2022

IJMS

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Acute respiratory distress syndrome (ARDS) consists of uncontrolled inflammation that causes hypoxemia and reduced lung compliance. Since it is a complex process, not all details have been elucidated yet. In a well-controlled experimental murine model of lipopolysaccharide (LPS)-induced ARDS, the activity and viability of macrophages and neutrophils dictate the beginning and end phases of lung inflammation. C-C chemokine receptor type 2 (CCR2) is a critical chemokine receptor that mediates monocyte/macrophage activation and recruitment to the tissues. Here, we used CCR2-deficient mice to explore mechanisms that control lung inflammation in LPS-induced ARDS. CCR2−/− mice presented higher total numbers of pulmonary leukocytes at the peak of inflammation as compared to CCR2+/+ mice, mainly by enhanced influx of neutrophils, whereas we observed two to six-fold lower monocyte or interstitial macrophage numbers in the CCR2−/−. Nevertheless, the time needed to control the inflammation was comparable between CCR2+/+ and CCR2−/−. Interestingly, CCR2−/− mice presented higher numbers and increased proliferative rates of alveolar macrophages from day 3, with a more pronounced M2 profile, associated with transforming growth factor (TGF)-β and C-C chemokine ligand (CCL)22 production, decreased inducible nitric oxide synthase (Nos2), interleukin (IL)-1β and IL-12b mRNA expression and increased mannose receptor type 1 (Mrc1) mRNA and CD206 protein expression. Depletion of alveolar macrophages significantly delayed recovery from the inflammatory insult. Thus, our work shows that the lower number of infiltrating monocytes in CCR2−/− is partially compensated by increased proliferation of resident alveolar macrophages during the inflammation control of experimental ARDS.

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Pulmonary macrophages and their different roles in health and disease

Cited by 16 publications

References 124 publications

The crosstalk between parenchymal cells and macrophages: A keeper of tissue homeostasis

The crosstalk between parenchymal cells and macrophages: A keeper of tissue homeostasis

Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species

Absence of CCR2 Promotes Proliferation of Alveolar Macrophages That Control Lung Inflammation in Acute Respiratory Distress Syndrome in Mice

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