11.3 Immunity to Bacteria and Fungi

Invasion, colonization, evasion of immunity, and tissue damage are the steps a microbe takes to cause disease.

Extracellular bacteria can replicate outside of host cells, such as in the blood, connective tissues, or the respiratory and gastrointestinal tracts.

The immune system's initial response to pathogens. It relies on cells like neutrophils, macrophages, NK cells, and complement proteins to fight off infection.

The specialized response of the immune system to specific pathogens, involving B cells, T cells, memory cells, and antibodies.

A critical part of the innate immune response, complement proteins activate the lysis (destruction) of bacteria.

Innate immune cells (e.g., neutrophils and macrophages) engulf and destroy extracellular bacteria using receptors like mannose, scavenger receptors, Fc receptors, and complement receptors.

A process where certain pathogens are able to evade or resist the immune response, allowing them to persist in the body.

Chronic infections where pathogens evade the immune system, often leading to long-term or recurrent disease.

Cells like phagocytes and dendritic cells release signaling molecules called cytokines during inflammation. Cytokines attract more immune cells to the infected area, amplifying the inflammatory response.

Innate lymphoid cells (ILCs) can be activated by an infection and release cytokines like IL-17 and IL-22. These cytokines act as signals, attracting immune cells like neutrophils to fight the infection.

Antibodies, especially IgG and IgA, play a crucial role in fighting extracellular bacteria. They work by binding to the bacteria, blocking their ability to infect cells and neutralizing their harmful toxins.

CD4+ helper T cells are important players in adaptive immunity against bacteria. They release cytokines, activate other immune cells, and stimulate antibody production, all to combat the infection.

Inflammation, while crucial for fighting off bacteria, can sometimes cause damage to healthy tissues due to the release of reactive oxygen species (ROS) and enzymes from immune cells. This damage is usually self-limiting, meaning it resolves on its own.

A severe infection that triggers a widespread inflammatory response, often leading to organ dysfunction. Caused by bacteria releasing toxins, activating immune cells, and causing a cascade of events with systemic effects.

Certain bacterial toxins that bind to MHC molecules, activating a large fraction of T cells, causing overwhelming immune activation.

Antibodies produced after a bacterial infection can sometimes mistakenly react with host tissues, causing autoimmune diseases. These antibodies are triggered by bacterial antigens that resemble certain human proteins.

Some bacteria possess a polysaccharide-rich capsule that protects them from phagocytosis by immune cells. This capsule acts as a shield, preventing the bacteria from being engulfed and destroyed.

Bacteria can change their surface antigens, making it difficult for the immune system to recognize and target them with antibodies. This allows them to persist and evade the immune response.

The immune system's first line of defense against intracellular bacteria involves phagocytes (like macrophages) and natural killer (NK) cells.

Toll-like receptors (TLRs) and NOD-like receptors (NLRs) are key sensors that detect bacteria within phagocytes, triggering an immune response.

Phagocytes release IL-12 and IL-15, which activate NK cells to target and kill infected cells.

The primary defense against intracellular bacteria involves the activation of T cells and phagocytes.

CD4+ T cells release CD40 ligand and IFN-γ, which help activate phagocytes to kill the bacteria.

CD8+ cytotoxic T lymphocytes (CTLs) directly kill infected cells, preventing the spread of bacteria.

Macrophage activation in response to intracellular bacteria can sometimes cause tissue damage, a potential consequence of the immune response.

Fungal infections are also known as mycoses, and many are opportunistic, meaning they cause disease in individuals with weakened immune systems.

The main cells involved in innate immunity against fungi are neutrophils, macrophages, and innate lymphoid cells (ILCs).

Certain protozoa can evade host immune responses by changing their surface antigens. They may express different antigens at various stages of their lifecycle. This is a common strategy used by parasites like malaria.

A type of immune evasion strategy where pathogens continuously shift their surface antigens, making it difficult for the immune system to target them effectively with antibodies.

The cytokine IFN-γ plays a crucial role in defending against various protozoal infections. It activates immune cells to clear the parasite infection.

The immune system relies on Th2 cells to combat helminth infections. These Th2 cells produce IgE antibodies, which attach to parasites. Eosinophils, activated by IL-5, bind to these IgE-coated parasites and release substances that kill them.

Parasitic antigens are often complex and can vary over time. This makes it challenging for the immune system to generate long-lasting immunity against some parasites.

Antigenic variation refers to viruses altering their surface antigens, evading host immune recognition. For example, influenza viruses use reassortment, a genetic shuffling mechanism, to rapidly change their antigens.

Viral inhibition of MHC molecules disrupts the presentation of viral antigens to T cells by infected cells, hiding the virus from the immune system.

Some viruses produce soluble cytokine receptors that bind to and neutralize key immune signaling molecules like IFN-γ, TNF, and IL-1, effectively dampening inflammatory responses.

Chronic viral infections often lead to T cell exhaustion, characterized by the upregulation of inhibitory receptors like PD-1 on T cells, making them less effective at fighting the infection.

Parasites, including protozoa and helminths, have evolved various strategies to evade or suppress the immune response, leading to chronic infections due to ineffective innate and adaptive immune responses.

Protozoa like Plasmodium spp. and Toxoplasma gondii can stimulate TLR2 and TLR4 receptors, leading to the activation of phagocytic cells in the innate immune response.

Eosinophils play a critical role in the innate immune response to helminths, while neutrophils and macrophages are less effective due to the parasites' thick tegument.

The adaptive immune response against parasites is tailored to the specific parasite type. For example, cell-mediated immunity, particularly macrophage activation by Th1 cells, is crucial for eliminating protozoa that reside within macrophages.

Bacteria that can replicate outside of host cells, such as in the blood, connective tissues, or the respiratory and gastrointestinal tracts.

The process by which pathogens evade or resist the immune response, allowing them to persist in the body.

Chronic infections where pathogens evade the immune system, often leading to long-term or recurrent disease.

A severe infection that triggers a widespread inflammatory response, often leading to organ dysfunction. Caused by bacteria releasing toxins, activating immune cells, and causing a cascade of events with systemic effects.

Certain bacterial toxins that bind to MHC molecules, activating a large fraction of T cells, causing overwhelming immune activation.

Antibodies produced after a bacterial infection can sometimes mistakenly react with host tissues, causing autoimmune diseases. These antibodies are triggered by bacterial antigens that resemble certain human proteins.

Some bacteria possess a polysaccharide-rich capsule that protects them from phagocytosis by immune cells. This capsule acts as a shield, preventing the bacteria from being engulfed and destroyed.

Bacteria can change their surface antigens, making it difficult for the immune system to recognize and target them with antibodies. This allows them to persist and evade the immune response.

Some bacteria possess a polysaccharide-rich capsule that protects them from phagocytosis by immune cells. This capsule acts as a shield, preventing the bacteria from being engulfed and destroyed.

Bacteria can change their surface antigens, making it difficult for the immune system to recognize and target them with antibodies. This allows them to persist and evade the immune response.

The main injurious effects of host responses to extracellular bacteria are inflammation which causes tissue damage by local production of ROS and lysosomal enzymes.

Some bacteria like to trick the immune system by changing their surface antigens. This constant change makes it hard for antibodies to target them, allowing them to escape the immune response. Think of a shape-shifting bacteria.

Certain bacteria have a protective capsule that hides them from phagocytes. This capsule prevents the immune cells from engulfing and destroying them. Imagine a bacteria wearing a protective shield.

Chronic viral infections can lead to T cells becoming exhausted, meaning they are less effective in fighting the infection.

Protozoa like Plasmodium spp. and Toxoplasma gondii can activate TLR2 and TLR4 receptors, leading to the activation of phagocytic cells in the innate immune response.

Intracellular bacteria, such as Mycobacterium tuberculosis and Salmonella, survive and multiply inside phagocytes, making them inaccessible to circulating antibodies.

Intracellular bacteria can evade the immune system by resisting phagocytosis, leading to persistent infections.

Fungal infections, also known as mycoses, are often opportunistic, affecting immunocompromised individuals. Fungi can live in extracellular tissues or inside phagocytes.

Cell-mediated immunity plays a key role in adaptive immunity against fungi, with CD4+ T cells activating macrophages and neutrophils for intracellular killing.

Viruses are obligate intracellular pathogens that replicate using the host's cellular machinery, often causing cytopathic effects.

The innate immune response to viruses involves type I interferons (IFN-α, IFN-β) that inhibit viral replication and NK cells that kill infected cells.

Adaptive immunity against viruses involves antibodies that block virus entry and CTLs that kill infected cells, preventing the spread of the virus.

A process where parasites alter their surface antigens, making it difficult for the immune system to recognize and destroy them.