It reduces inflammation causing enzymes

Also stabilises cell membrane

It calms down immune response to reduce pain, swelling.

• It binds to the glucocorticoid receptor, translocates to the nucleus, and modulates the transcription of inflammatory genes.

• It inhibits key enzymes like PLA2 and COX-2, reducing the production of inflammatory mediators such as prostaglandins and leukotrienes.

• It suppresses pro-inflammatory cytokine production and immune cell activation, reduces the recruitment of immune cells to inflamed tissues, and induces apoptosis in certain immune cells. These combined actions make hydrocortisone an effective treatment for inflammatory conditions such as arthritis, asthma, and autoimmune disorders.

✅ NF-κB (Nuclear Factor Kappa B): Hydrocortisone blocks NF-κB, reducing pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6.

✅ IL-1β, IL-6, TNF-α: These cytokines cause inflammation; hydrocortisone lowers their levels.

✅ Annexin-1: Hydrocortisone activates this anti-inflammatory protein, which stops PLA2 (phospholipase A2) from making prostaglandins.

✅ CRP (C-reactive protein): Hydrocortisone reduces CRP levels, lowering systemic inflammation.

🎯 Effect: Less redness, swelling, and itching in dermatitis.

Hydrocortisone enters cells and binds to specific glucocorticoid receptors, triggering changes in gene expression.

Anti-inflammatory effects:

By modulating gene expression, hydrocortisone reduces the production of inflammatory molecules like prostaglandins and leukotrienes, which are responsible for swelling and pain.

Immune suppression:

It also suppresses the activation and proliferation of immune cells like T lymphocytes and B lymphocytes, further limiting inflammation.

Vascular effects:

Hydrocortisone can decrease capillary permeability and reduce leukocyte migration to inflamed sites, minimizing swelling.

Metabolic effects:

At high doses, hydrocortisone can influence metabolism by affecting blood sugar levels and proteinprotein.

Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.

Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10.

Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive.

High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.

Function

Hydrocortisone has several functions:

1. Anti-inflammatory: Reduces inflammation and swelling by suppressing the immune system's response.

2. Immunosuppressive: Decreases the activity of the immune system, which can help alleviate conditions like allergies, asthma, and autoimmune disorders.

3. Vasoconstrictive: Narrows blood vessels, reducing blood flow to affected areas and alleviating symptoms like redness and itching.

Effects

The EFFECTS of hydrocortisone depend on the specific condition being treated:

1. Skin conditions: Relieves inflammation, itching, and redness associated with eczema, dermatitis, and psoriasis.

2. Allergic reactions: Reduces symptoms like hives, itching, and swelling.

3. Respiratory issues: Helps alleviate asthma symptoms, such as wheezing and shortness of breath.

4. Gastrointestinal issues: May be used to treat conditions like ulcerative colitis and Crohn's disease.

How it WORKS ?

Hydrocortisone works by:

1. Binding to glucocorticoid receptors: Hydrocortisone binds to specific receptors in cells, triggering a response that reduces inflammation and immune activity.

2. Suppressing inflammatory genes: Hydrocortisone decreases the production of pro-inflammatory genes, leading to reduced inflammation and immune response.

3. Stabilizing cell membranes: Hydrocortisone helps maintain cell membrane integrity, reducing the release of inflammatory chemicals.

The short-term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation.¹⁰ Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.¹⁰

Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10.¹⁰

Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive.¹⁰ High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.¹⁰

Wheezing, difficulty breathing, or chest pain

Drop in blood pressure

Fatigue

Infections

Fever or sore throat

Blood in stool, black or tarry stools, or bloody or cloudy urine

Infections like anemia, leukopenia, neutropenia, and thrombocytopenia

Liver problems itchy skin, yellowing of the skin or eyes, dark-brown urine, pain in the upper right part of the stomach, and loss of appetite.

Other side effects

Headaches, Dizziness, Flushing, Stomach pain, Indigestion, and Feeling sick.

You should contact your doctor immediately if you experience any of these side effects.

1. Infusion reactions (fever, chills, rash).

2. Increased risk of infections (TB, fungal, bacterial).

3. Autoimmune responses (lupus-like symptoms, blood disorders).

4. Worsening heart failure and hypotension.

5. Slightly increased cancer risk (lymphoma, skin cancer).

6. Liver issues (hepatotoxicity).

7. Potential worsening of IBD.

Headache

Coughing

Stomach pain

Respiratory infections, like sinus infections or sore throat

Belching

Heartburn

Indigestion

Muscle stiffness

Redness of the face, neck, arms, and sometimes upper chest

Serious side effects

Allergic reactions, including delayed reactions

Lupus-like syndrome

Psoriasis

Cancers, including lymphoma and skin cancer

Heart attack

Stroke

Changes in blood pressure

Heart rhythm problems

Infusion reactions

chest pain, fever, chills, itching, hives, rash, dizziness, fainting, lightheadedness, and joint pain.

• Serious infections: There is an increased risk of severe infections, including tuberculosis, bacterial sepsis, and invasive fungal infections. ...

• Malignancy: Lymphoma and other malignancies, some fatal, were documented in children and adolescents treated with TNF blockers, including infliximab

Neurological problems

Risk of heart failure

2. Autoantibody production: Infliximab can induce the production of autoantibodies, leading to autoimmune reactions.

3. Cytokine imbalance: Infliximab's disruption of the cytokine balance can lead to an increased risk of malignancies.

4. Neurotransmitter modulation: Infliximab can modulate neurotransmitter activity, leading to neurological problems.

It also kills immune cells

Risk of cancer. Reduce wound healing

Infliximab injection is also used to treat chronic severe (extensive or disabling) plaque psoriasis, which is a skin disease with red patches and white scales that do not go away. It is used in patients who cannot be treated with other medicines.

Infliximab is a monoclonal antibody that works to enhance and improve the immune system.

painful or difficult urination

pale skin

pounding in the ears

runny or stuffy nose

slow or fast heartbeat

sneezing

sore throat

sores, ulcers, or white spots on the lips or in the mouth

stomach pain

tender, swollen glands in the neck

tightness in the chest

trouble breathing

trouble swallowing

2. Opsonisation – It binds to the surface of dead or dying cells, as well as some bacteria, marking them for clearance by immune cells such as macrophages.

3. Complement System Activation – CRP can activate the complement pathway, enhancing the body’s ability to destroy pathogens and remove cellular debris.

4. Inflammatory Regulation – It interacts with immune cells to modulate the inflammatory response, either promoting or limiting inflammation depending on the situation.

5. Clinical Marker of Inflammation – High levels of CRP in the peripheral blood indicate systemic inflammation and are used in diagnosing infections, autoimmune diseases, and cardiovascular conditions.

Molecular Basis:

CRP is a pentameric protein composed of five identical subunits. Each subunit has a binding site for phosphocholine.

1. Binding to phosphocholine: CRP binds to phosphocholine through a calcium-dependent interaction, which allows it to recognize and bind to pathogens.

2. Activation of complement system: CRP binds to the complement component C1q, activating the classical complement pathway and leading to the elimination of pathogens.

3. Interaction with Fc receptors: CRP binds to Fc receptors on the surface of immune cells, such as neutrophils and macrophages, enhancing their phagocytic activity.

4. Modulation of cytokine activity: CRP can bind to cytokines, such as TNF-alpha, and modulate their activity, which helps to regulate the inflammatory response.

Clinical Significance:

CRP is used as a biomarker for inflammation and infection. Elevated CRP levels are associated with various conditions, including:

- Infections (e.g., pneumonia, sepsis)

- Inflammatory diseases (e.g., rheumatoid arthritis, lupus)

- Cardiovascular disease

- Cancer

In summary, CRP plays a vital role in the immune response, recognizing pathogens, activating the complement system, enhancing phagocytosis, and modulating inflammation. Its molecular basis involves binding to phosphocholine, interacting with complement components, Fc receptors, and cytokines.

1. Marking pathogens and damaged cells for removal by immune cells.

2. Activating the complement system to fight infections.

3. Regulating inflammation and promoting tissue repair.

4. Elevated CRP levels indicate ongoing inflammation or infection and can increase the risk of cardiovascular events.

It’s commonly used as a marker of inflammation in the body.

1. *Recognition of pathogens*: CRP binds to phosphocholine, a component of bacterial cell walls, helping to recognize and eliminate pathogens.

2. *Activation of complement*: CRP activates the complement system, a group of proteins that work together to eliminate pathogens.

3. *Enhancement of phagocytosis*: CRP helps to facilitate the engulfment and destruction of pathogens by phagocytic cells.

*Role in Inflammation*

1. *Induction of pro-inflammatory cytokines*: CRP induces the production of pro-inflammatory cytokines, such as TNF-α and IL-6.

2. *Recruitment of immune cells*: CRP helps to recruit immune cells, such as neutrophils and macrophages, to the site of inflammation.

3. *Increased vascular permeability*: CRP contributes to increased vascular permeability, allowing immune cells and fluids to reach the site of inflammation.

*Role in Tissue Repair*

1. *Clearance of apoptotic cells*: CRP helps to clear apoptotic cells, which is essential for tissue repair and regeneration.

2. *Modulation of fibrosis*: CRP can modulate the development of fibrosis, a condition characterized by excessive scarring.

*Role in Cardiovascular Disease*

1. *Endothelial dysfunction*: Elevated CRP levels are associated with endothelial dysfunction, a precursor to atherosclerosis.

2. *Atherogenesis*: CRP may contribute to the development of atherosclerosis by promoting the uptake of lipids by macrophages.

In summary, CRP plays a multifaceted role in the peripheral body, contributing to the recognition and elimination of pathogens, the induction of inflammation, tissue repair, and the development of cardiovascular disease.

1. Opsonization & Complement Activation

- CRP binds to phosphocholine on the surface of pathogens and damaged cells.

- This binding tags (opsonizes) these targets for phagocytosis by macrophages and neutrophils.

- CRP activates the classical complement pathway, leading to immune clearance.

2. Inflammation Regulation

- CRP interacts with immune cells, promoting the release of pro-inflammatory cytokines (IL-6, TNF-α).

- It recruits immune cells to sites of injury or infection.

- In chronic conditions, elevated CRP contributes to persistent inflammation (e.g., cardiovascular disease, rheumatoid arthritis).

3. Cardiovascular Effects

- CRP is linked to atherosclerosis by promoting:

- Endothelial dysfunction

- Foam cell formation (via LDL oxidation)

- Plaque instability and thrombosis

4. Role in Autoimmune and Chronic Diseases

- CRP is elevated in autoimmune diseases like rheumatoid arthritis, lupus, and inflammatory bowel disease (IBD).

- It serves as a biomarker of disease activity and treatment response.

5. Infection Response

- CRP levels rise rapidly (within 6–8 hours) during bacterial infections, making it a useful diagnostic marker for sepsis or pneumonia.

- It helps differentiate bacterial infections (high CRP) from viral infections (low CRP).

• Vascular endothelial cells (blood vessels)

• Adipose tissue (fat cells)

• Smooth muscle cells

• Macrophages and monocytes

• Kidneys and lungs

Tissue repair

Opsonisation by binding to pathogens and marking them for destruction

Endothelial functions by increasing expression of adhesion molecules such as ICAM-1 and VCAM-1

1️⃣ Liver Production: IL-6, TNF-α, and IL-1β activate the liver to make CRP.

2️⃣ Opsonization: CRP attaches to bacteria, viruses, and damaged cells. This helps macrophages and neutrophils to find and destroy them.

3️⃣ Complement System Activation: CRP activates the classical complement pathway (C1q),helping the immune system to remove infections and reduce inflammation.

2. Tissue damage: CRP contributes to tissue damage by activating inflammatory cells and promoting the release of destructive enzymes.

1. Endothelial dysfunction: CRP can impair endothelial function, leading to reduced vasodilation and increased blood pressure.

2. Increased vascular permeability: CRP can increase vascular permeability, allowing fluid and inflammatory cells to leak into tissues, leading to edema and inflammation.

3. Enhanced inflammatory response: CRP can amplify the inflammatory response by binding to Fc receptors on immune cells, leading to increased production of pro-inflammatory cytokines.

4. Tissue damage: CRP can contribute to tissue damage by promoting the formation of reactive oxygen species (ROS) and activating matrix metalloproteinases (MMPs).

5. Impaired wound healing: Elevated CRP levels can impede wound healing by reducing collagen synthesis, impairing tissue remodeling, and increasing the risk of infection.