Macrophages play important roles in all stages of wound healing. Changes in micro-environment leads to transformation of macrophages type I and type II, thereby playing a role in wound healing. During the early inflammatory phase, type I macrophages exert pro-inflammatory function such as antigen-presenting, phagocytosis, and the production of inflammatory cytokines and growth factors. While during the wound healing phase, macrophages were transformed into type II, which stimulate the proliferation of fibroblasts, keratinocytes, and endothelial cells by expressing growth factors. This results in the formation of granulation tissue, angiogenesis, and the formation of ECM, so as to promote wound healing. This review summarizes the function and change in phenotype of macrophages in different stages of wound healing.
Humans ; Macrophages ; immunology ; Wound Healing ; immunology

Despite the evolution of aggressive surgical techniques, extensive methods of supportive care and a vast array of anti-microbial options, intra-abdominal infection (IAI) is still a challenging clinical issue. Especially, when progressed IAI with septic complications because of unbalanced immune responses, the prognosis will deteriorated significantly. Recent studies indicate that besides the natural immunological cells, including macrophages and neutrophils, local immunological characteristics of peritoneal cavity should be studied with great attention. Among them, the omentum is considered to be a visceral adipose tissue with unique immune function. The milky spots(MSs) formed by the accumulation of immune cells performs immune surveillance and has a lymph node-like immune function, which is very important for the immune defense of the abdominal cavity. B1 cells and two types of intrinsic lymphocytes(ILC2) in the peritoneal cavity, although belonging to the lymphatic lineage, may play an important role in abdominal infections, especially in the early stages of the disease, due to their rapid responsiveness and acquired immune function. Therefore, paying attention to the immunological characteristics of the peritoneal cavity, and elucidating the changes, functions and regulatory mechanisms of B1 cells and ILC2 around the MSs and their components in the process of IAI, in order to explore the immunomodulation targets of blocking the infection from local to systemic dissemination, may be the key to solving the clinical problem of severe IAI and improving prognosis.
Humans ; Intraabdominal Infections ; immunology ; Lymphocytes ; immunology ; Macrophages ; immunology ; Omentum ; immunology ; Peritoneal Cavity

Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages (HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6 by HMDM. The involvement of nuclear factor (NF)-kappaB signaling pathway in cytokine production induced by T. vaginalis was confirmed by phosphorylation and nuclear translocation of p65 NF-kappaB. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide (NO) production and expression of inducible NO synthase (iNOS) levels in HMDM. However, trichomonad-induced NF-kappaB activation and TNF-alpha production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA (NO synthase inhibitor). Moreover, pretreatment with NF-kappaB inhibitors (PDTC or Bay11-7082) caused human macrophages to produce less TNF-alpha. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, and NO. In particular, we showed that T. vaginalis induced TNF-alpha production in macrophages through NO-dependent activation of NF-kappaB, which might be closely involved in inflammation caused by T. vaginalis.
Animals ; Cells, Cultured ; Cytokines/*immunology ; Humans ; Macrophages/*immunology/parasitology ; Nitric Oxide/*immunology ; Trichomonas Infections/*immunology/parasitology ; Trichomonas vaginalis/*immunology

Trichomonas vaginalis commonly causes vaginitis and perhaps cervicitis in women and urethritis in men and women. Macrophages are important immune cells in response to T. vaginalis infection. In this study, we investigated whether human macrophages could be involved in inflammation induced by T. vaginalis. Human monocyte-derived macrophages (HMDM) were co-cultured with T. vaginalis. Live, opsonized-live trichomonads, and T. vaginalis lysates increased proinflammatory cytokines, such as TNF-alpha, IL-1beta, and IL-6 by HMDM. The involvement of nuclear factor (NF)-kappaB signaling pathway in cytokine production induced by T. vaginalis was confirmed by phosphorylation and nuclear translocation of p65 NF-kappaB. In addition, stimulation with live T. vaginalis induced marked augmentation of nitric oxide (NO) production and expression of inducible NO synthase (iNOS) levels in HMDM. However, trichomonad-induced NF-kappaB activation and TNF-alpha production in macrophages were significantly inhibited by inhibition of iNOS levels with L-NMMA (NO synthase inhibitor). Moreover, pretreatment with NF-kappaB inhibitors (PDTC or Bay11-7082) caused human macrophages to produce less TNF-alpha. These results suggest that T. vaginalis stimulates human macrophages to produce proinflammatory cytokines, such as IL-1, IL-6, and TNF-alpha, and NO. In particular, we showed that T. vaginalis induced TNF-alpha production in macrophages through NO-dependent activation of NF-kappaB, which might be closely involved in inflammation caused by T. vaginalis.
Animals ; Cells, Cultured ; Cytokines/*immunology ; Humans ; Macrophages/*immunology/parasitology ; Nitric Oxide/*immunology ; Trichomonas Infections/*immunology/parasitology ; Trichomonas vaginalis/*immunology

Non-Hodgkin's lymphoma cells including lymphoma stem cells reside in a specific microenvironment in which a series of nonmalignant bystander cells and cytokines play a crucial role in the genesis and development of non-Hodgkin's lymphomas. In addition, tumor microenvironment has important prognostic significance in Non-Hodgkin's lymphomas. Blocking the cross-talk between the tumor microenvironment and lymphoma cells may thus represent a promising new strategy for treating Non-Hodgkin's lymphomas. This review summarizes the current advance in studies of the tumor microenvironment and non-Hodgkin's lymphomas, including cells in tumor microenvironment, role of mesenchymal stem cells and stromal cells, auxiliary role of T cell subsets, macrcphage and dentritic cells, cytokines, immune surveillance and so on.
Cytokines ; immunology ; Dendritic Cells ; immunology ; Humans ; Lymphoma, Non-Hodgkin ; immunology ; Macrophages ; immunology ; T-Lymphocyte Subsets ; immunology ; Tumor Microenvironment

The immune microenvironment plays an important role in the occurrence and development of breast cancer. The infiltrating immune cells and the produced inflammatory cytokines in the tumor microenvironment regulate the growth, proliferation and metastasis of breast cancer. In this article, the roles and related mechanisms of nonspecific immune microenvironment in breast cancer are summarized, focusing on the natural killer cells, dendritic cells, myeloid derived suppressor cells, tumor associated macrophages, interleukins, chemokines, tumor necrosis factor-α, transforming growth factor-β and so on.
Breast Neoplasms ; immunology ; physiopathology ; Chemokines ; immunology ; Dendritic Cells ; immunology ; Humans ; Macrophages ; immunology ; Research ; trends ; Tumor Microenvironment ; immunology

Mycobacterium tuberculosis (Mtb) is an intracellular pathogen that infects alveolar macrophages following aerosol transmission. Lung macrophages provide a critical intracellular niche that is required for Mtb to establish infection in the human host. This parasitic relationship is made possible by the capacity of Mtb to block phagosome maturation following entry into the host macrophage, creating an environment that supports bacillary replication. Apoptosis is increasingly understood to play a role in host defense against intracellular pathogens including viruses, fungi, protozoa and bacteria. In the last 15 years an understanding of the role that macrophage apoptosis plays in TB has begun to emerge. Here we review the history and current state of the art of this topic and we offer a model of the macrophage-pathogen interaction that takes into the account the complexities of programmed cell death and the relationship between various death signaling pathways and host defense in TB.
Animals ; Apoptosis/*immunology ; Humans ; Macrophages/*cytology/*microbiology ; Mycobacterium tuberculosis/*immunology ; Tuberculosis, Pulmonary/*immunology

The review summarized the recent progress on macrophages of male reproductive tract and the action of macrophages on male reproductive physiology and pathology. The close correlation and effect between testicular macrophages and Leydig cells, Sertoli cells, germ cells, hypothalamic-pituitary-gonadal axis were introduced, respectively. At the same time, it pointed out the changes of macrophages' morphology and function in immune orchitis, and their regulation on the development of orchitis. So the complex immune regulation network in testes and testicular macrophages playing an important role on spermatogenesis and the stableness of spermatogenetic microenvironment in testes were further illuminated, which can provide theoretical basis for clinic therapy.
Genitalia, Male ; cytology ; immunology ; physiology ; Humans ; Macrophages ; cytology ; immunology ; Male ; Orchitis ; immunology ; pathology ; Spermatogenesis ; physiology

As a result of the stimulation of proinflammatory mediators, circulating peripheral-blood mononuclear cells migrate into the wound area, and they differentiate into different phenotypes of macrophage to take different roles in healing process. Their phenotypes interchange under different microenvironments. The disturbance of cutaneous environment in diabetic patients has been shown to alter the quantity, morphology, and functions of the macrophages resulting in retardation of wound healing. Healing of intractable diabetic wound can be improved by the supplement of exogenous growth factors, which might improve healing process by regulating the phenotype of macrophage in intractable diabetic wound. This article reviews the relationship between intractable diabetic wound and macrophage to explore new methods of treating intractable diabetic wound.
Diabetes Mellitus ; immunology ; metabolism ; Humans ; Macrophages ; physiology ; Skin ; Wound Healing

OBJECTIVE: The aim of this study was to investigate the effect of saliva of patients with chronic periodontitis (CPD) on the differentiation, activation, and secretion of osteoclast-maturing mediators of macrophages. METHODS: A total of 40 saliva samples were collected from healthy donors (n=20) and severe periodontitis patients (n=20). Peripheral blood mononuclear cells (PBMCs) and THP-1 monocyte line cells were challenged with 15% saliva for 5 days. The phenotype, surface marker, and phagocytosis of macrophages were analyzed by flow cytometry and microscopy. Osteoclast-maturing mediators were assayed by using enzyme-linked immunosorbent assay (ELISA) kits. RESULTS: When PBMCs were treated with CPD saliva for 5 days, 61.25%±11.33% of cells were transformed into large granular cells; 86.78%±13.69% of large granular cells were identified as CD14⁺⁺CD16⁺ macrophages. When THP-1 cells were treated with CPD saliva, most cells attached to the bottom of cell culture plates, thereby exhibiting macrophage morphology and releasing additional osteoclast-maturing mediators. Furthermore, the phagocytosis of THP-1 cells considerably increased in the presence of CPD saliva (66.35%±9.67%) compared with medium control (33.33%±7.52%), or healthy saliva (40.71%±3.52%). CONCLUSIONS Saliva from patients with CPD can induce macrophage differentiation, activate phagocytose microorganisms, and secrete osteoclast-maturing mediators.
Cell Differentiation ; Humans ; Leukocytes, Mononuclear ; Macrophages ; Monocytes ; Periodontitis ; immunology ; Saliva