Chronic inflammation, known as prolonged inflammation, leads to a progressive shift in the type of cells present at the site of inflammation and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process.
On the other hand, acute inflammation (Pic. 1) is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (white blood cells) from the blood into the injured tissues.
If the injurious agent persists in acute inflammation, then chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterised by the dominating presence of macrophages (white blood cells) in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species; ROS) are injurious to the organism's own tissues as well as invading agents. As a consequence, chronic inflammation is almost always accompanied by tissue destruction.
There isn’t a highly effective laboratory measure to assess patients for chronic inflammation. It really is a diagnosis by process of elimination – which means other possibilities must be ruled out. Drugs that can help address chronic inflammation including anti-inflammatory drugs. Moreover, several dietary and lifestyle changes can help reduce chronic inflammation.
Chronic inflammation during pregnancy
Several maternal insults during pregnancy are known as major cause of fetal brain damage, including infection. Maternal insult is associated with morbidity and mortality to infants and other complications. It is suggested that brain damage of offspring, which belong to mothers who have suffered of intrauterine infection/inflammation during pregnancy, is mediated by toxicity for nervous system. The mechanisms or pathophysiology of fetal neurotoxicity, induced by insult exposure are complex and not fully understood. Chronic diseases may also lead to increasing possibility of early pregnancy loss.
Dietary changes and lifestyle modifications can go a long way in helping the body reduce its inflammation production, and in the case of autoimmune conditions, stop attacking itself. Moreover, enough sleep and preventing stress may help to reduce risk of chronic inflammation.
Inflammation can contribute to infertility in two ways. On its own, inflammation can damage cells and tissues in the reproductive organs, such as eggs, ovaries, or sperm. Chronic inflammation can also be connected to an autoimmune response, in which the body attacks its own tissue via antibodies. People with autoimmune conditions are more susceptible to these complications, and it is even more important for them to work on decreasing inflammation in every way possible.
Unexplained infertility is defined as the inability to conceive after 12 months of unprotected intercourse in couples where known causes of infertility have been ruled out. It is thus considered a diagnosis of exclusion. Its pathophysiology remains unclear, although the literature suggests a possible contribution by increased levels of oxidative stress. Inflammation and oxidative stress are closely related and tightly linked pathophysiological processes. As the inflammatory process can induce oxidative stress, the oxidative stress can also induce inflammation through activation of multiple pathways.
Infection is also a major factor in male subfertility, second only to abnormal semen parameters. Epididymal or ductal obstruction, testicular damage from orchitis, development of anti-sperm antibodies, etc are all possible mechanisms by which infection can affect male fertility.
In males, the role of oxidative stress (imbalance between production and accumulation of oxygen reactive species (ROS)) in pathologies has long been recognized as a significant contributor to infertility. The key predictors of fertilization capability are sperm count and motility. These essential factors can be disturbed by ROS and much importance has been given to oxidative stress as a major contributor to infertility in males.
Chronic inflammation of the cervix and endometrium, alterations in reproductive tract secretions, induction of immune mediators that interfere with gamete or embryo physiology, and structural disorders such as intrauterine synechiae all contribute to female infertility.
Inflammation leads to anatomic disorders primarily as a result of infectious disease; including polycystic ovary syndrome (PCOS), endometriosis (inflammation of inner lining of the uterus), recurrent miscarriage, and premenstrual syndrome (PMS).
The contribution of oxidative stress to male infertility has been well documented and extensively studied. On the other hand, the role of oxidative stress in female infertility continues to emerge as a topic of interest, and thus, the majority of conducted studies provide indirect and inconclusive evidence regarding the oxidative effects on female reproduction.
Approximately 35% of women with an infertility problem are afflicted with post-inflammatory changes of the oviduct or surrounding peritoneum that interfere with tubo-ovarian function. Most of these alterations result from infection. Salpingitis occurs in an estimated 15% of reproductive-age women, and 2.5% of all women become infertile as a result of salpingitis by age 35.
The relationship between brain damages of offspring following maternal infection/inflammation during pregnancy is not yet clear. Therefore, some of the suggested therapeutic possibilities are based on possible mechanisms of the offspring brain damages.
Since the chronic inflammation could impair the fertility potential, it is neccessary to treat the condition. The long-term consequences of prolonged inflammation depend on the duration of the disease and thus the fertility outcomes could be variable by individual case.